Is DNA from more parents (than two) better for the fitness of the offspring?

Is DNA from more parents (than two) better for the fitness of the offspring?

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I'm designing a system (a computer system actually) and (a whole while ago) I spoke with a friend about it and he had this opinion:

If you combine DNA of more parents (than 2) it's better for the offspring.

It's a bit of a theoretical question but is this true?

I'm using genetic algorithms where you can choose the number of parents, if this were to be true I'd take 4 parents, if not I'd stick to 2.

I saw here a question about the occurrence in nature but it remains unanswered.

(2 parents are easier - in this system - so maybe that's the reason it is not observed in nature)

About the system: it needs to produce 'fit' offspring (as fit as possible and as fast as possible), where fitness is measurable (this part is already covered… ) and the most fit individuals in the population are selected to pair.

The only limitation set on this kind of systems is that the offspring has to have a chance to be fitter than the parents (so children are allowed to be less fit than parents (being it 4 or 2).

(Of course this lowers the importance of the question but still: does offspring of more than 2 parents have a higher chance to be fit? (my friend mentioned: the more diversity in the DNA the better… ))

If you need more information about this bit I'll try to answer comments (if I do know the answer or can give more information about it).

There are very many details to address in this question. I will try to keep it brief and keep the scope of your question in mind, which is rather narrow. I also think your friend is over-simplifying and misleading you, assuming he is honest about the explanation he gave you.

We are talking about sexual reproduction, correct? Firstly, with 3+ parents:

  • it's not obvious that you will have "more diversity" in the DNA, nor that
  • "more diverse" DNA will be a cause for increased fitness.
  • Additionally, it would take a whole lot of machinery and evolutionary happenstance at the cellular and molecular levels to recombine DNA from 3 or more parents to make a stable, recombined genome, and this itself may introduce more problems than solutions.
  • More so, you're implying that a sexual organism that requires mating between 3 or more individuals will be fitter than an organism born of fewer parents. This is subject to whether the gain in fitness of having more genetic parents will outweight the cost of maintaining such a system. This would certainly be dependent on the environment, the population, and all the nasty little details of life, such as how mate choice would work, whether a backup for 2-individual mating would exist, etc.

Remember that fitness is a probability of obtaining a number of offspring rather than the number of offspring. I think it is self-evident that the requirement for more parents, rather than less, lowers the probability (i.e. fitness).

This is quite a hypothetical discussion. In nature, for all its ever-experimenting and ever-diverging forms of life in the last 4 billion years, we find no organisms with more than 2 sexual parents. Take this as a sign that the natural occurrence of this kind of system is probably not favorable to survival and reproduction.

And I realize we could discuss this topic on many fronts (I have a few more ideas that I omit here), it's a rich question to digest.

What donor offspring seek when they do DNA testing

I wrote previously about parents who fear that their donor-conceived children might uncover long-held secrets through DNA testing. Many were unsettled by Dani Shapiro’s memoir Inheritance, which told of how a DNA test done for no particular reason dismantled a family story. Now let’s consider reasons why some people who know they were donor-conceived might pursue DNA testing.

Why might people who were donor-conceived seek DNA testing?

Donor-conceived adults who embark upon DNA testing may, like Shapiro, stumble upon information accidentally. Their experience with DNA testing is not explored in this post, which focuses on those whose choice to do testing followed one of these three paths:

  • They were told their conception story at a young age, but had limited information about their donor and his or her family.
  • They were only recently told of their donor conception, but grew up knowing something was different or left unspoken (the “unknown known”).
  • As adults, they were completely startled to learn that they were donor-conceived.

What might people hope to learn through DNA testing?

So what might these people seek — and hope to find — in DNA testing? Everyone is different and DNA testers have a wide range of reasons for swabbing their cheeks. Yet most have the desire to better understand their personal story. We all have origin stories that circle around our ancestry, ethnicity, and the circumstances of our conception and birth. Whether they grow up always knowing, or learn of donor conception as young adults, personal stories for the donor-conceived are complicated. Questions people hope to have answered include:

  • Why did he or she become a donor? Am I simply the product of a transaction, or were there other reasons that motivated someone to donate?
  • Who else am I related to? This question is especially compelling for sperm donor offspring, who may have large numbers of genetic half-siblings. This is less often true for those conceived from donated eggs, yet there are the donor’s children, her nieces and nephews, all those she donated to, and in some instances, children born through embryos donated to other families after the original recipient family was complete.
  • What is my ethnicity? What does it mean if the ethnicity in my DNA does not match the ethnic identity I was raised with? One woman I spoke with had grown up believing she was Irish on her mother’s side and Jewish (Ashkenazi) on her dad’s side. When the DNA test results came back indicating she is 100% Irish, she felt a sense of loss. She always felt proud to be half Jewish. Did this mean that she is not?
  • What abilities and vulnerabilities might I have inherited from the donor? For many, the high beam of this question directs itself to medical issues. This can go both ways: learning one’s actual medical history may relieve worries regarding illnesses in the family, or it may bring new medical concerns. Either way, those who are just learning they were donor-conceived as adults have relied on a family medical history that they now know to be only half complete.
  • Most people feel they came from two people. I came from three. What does this mean for my identity? People conceived with donated eggs are often, though not always, told of the donation from a young age. They grow up always knowing that they are gestationally, but not genetically, connected to their mothers. Part of their task as they mature is sorting out as best they can what it means to literally come from three people. (Sperm donor offspring, by contrast, must reconcile with the fact that they have no physical connection to their fathers.)

What does the future hold?

The world of commercially available DNA testing is still in its infancy. These days it is being heavily marketed in the media as a nifty gift, an interesting tool, a key that will unlock doors. Undoubtedly its uses, and its meaning for all of us, will unfold and evolve over time. The questions it raises and the “answers” it provides are surely more complex and multidimensional for the donor-conceived.

For more information

If you’d like further information and support, you may find these organizations helpful.

Coral offspring physiology impacted by parental exposure to intense environmental stresses

Adult corals that survive high-intensity environmental stresses, such as bleaching events, can produce offspring that are better suited to survive in new environments. These results from a series of experiments conducted at the Bermuda Institute of Ocean Sciences (BIOS) in 2017 and 2018 are deepening scientists' understanding of how the gradual increase of sea surface temperatures and other environmental disturbances may influence future coral generations.

Researchers on the project included BIOS marine ecologists Samantha de Putron and Gretchen Goodbody-Gringley (now with the Central Caribbean Marine Institute), ecophysiologist Hollie Putnam at the University of Rhode Island (URI), and Kevin Wong, then a first-year doctoral student at URI. Primary funding came from the Heising-Simons Foundation International, Ltd. with additional funding from the National Geographic Society and the Canadian Associates of BIOS (CABIOS).

The team spent last year working the data into a manuscript, which was published this month in the journal Global Change Biology and listed Wong as the first author. Wong, now nearing the end of his fourth year of studies at URI under the mentorship of Putnam, plans to graduate in May 2022.

"We know parental history influences the characteristics of offspring in corals, however the experimental design used in this study provides us with a unique perspective on how multiple types of thermal events can accumulate over time and have lasting consequences across generations," Wong said.

Coral Collection and Study

The multi-year field and lab-based study began in the summer of 2017. Departing from BIOS on a small boat with diving gear, the team collected 40 adult Porites astreoides (mustard hill) corals from two different reef sites northwest of Bermuda: a patch reef (Crescent Reef), which is located in a shallower lagoon environment, and a rim reef (Hog Reef) which is a barrier reef more exposed to open ocean conditions.

They next placed the live corals in the then newly-constructed BIOS mesocosm facility, where large outdoor aquaria "flow-through" seawater systems allowed researchers to control and adjust water temperature in the tanks for completing the study.

A variety of baseline data were collected on the corals in each colony, such as metabolic rates and the density of Symbiodinaceae, the symbiotic algae that live within the coral tissues. To simulate a thermal stress event, the adult corals were exposed to two different temperature treatments -- ambient (84°F or 29°C) or heated (88°F or 31°C) -- for a period of 21 days over their reproductive period. Afterward, the team assessed the physiology of the adult corals, looking at key functions such as respiration and photosynthetic rates. They also monitored the release of coral larvae and assessed its physiology, measuring the larval size and density of Symbiodinaceae within each larva, among other factors.

Upon completion of the experiment, the adult corals were divided in half and reciprocally transplanted, with half of the fragments positioned in the new environments and half returned to their originating environments. All of the fragments remained in place until the summer of 2018, when they were re-collected, and the physiologies of both adult corals and coral larvae were assessed in the same manner as in 2017.

A Stronger Coral Generation

The results of this two-year investigation showed that adult corals that experienced the thermal stress event produced offspring more capable of thriving in their current environment. This means that parent corals that experience stressors may be able to "pre-condition" their offspring to survive in new environments in the following year. The results also indicate that high-intensity environmental stress events, such as bleaching, can have lasting impacts on adult colonies and how they produce their offspring.

"The coral used in this study is a notoriously resilient coral and these findings potentially demonstrate how this species is so persistent across the Caribbean," Putnam said. "Not all coral species are this robust to environmental stressors. However, this system allows us to unravel the mechanisms leading to resilience and identify which corals are most sensitive to climate change."

Long-time Member of BIOS Community

Wong, 27, is a familiar face at BIOS, having first arrived on campus in the summer of 2014 as a CABIOS intern when he spent 12 weeks working with de Putron on a research project investigating the role of temperature and light on the growth and survivorship of juvenile mustard hill corals from two different reef zones. The following year, he received CABIOS funding to work with then-faculty member Gretchen Goodbody-Gringley on a project focused on the reproductive ecology of corals from mesophotic reef ecosystems, deeper-water reefs which typically extend from 100 to almost 500 feet (30 to 150 meters) in depth.

While presenting the results of his research at the 2016 International Coral Reef Symposium meeting in Hawaii, he had the opportunity to interview with Putnam for URI's Biological and Environmental Sciences doctoral program. Wong then returned to BIOS to spend six months in 2016 as a teaching assistant for several summer and fall courses. He also received BIOS Grants-in-Aid funding for a research project with Goodbody-Gringley and de Putron focused on the reproductive ecology of mustard hill coral from various reef sites around Bermuda, resulting in a publication in the journal Coral Reefs.

"It is wonderful to see an undergraduate intern progress to a successful graduate student who is publishing manuscripts," de Putron said. "Many years of hard work and plenty of exhausting, yet fun, days in the field and laboratory all culminated in interesting and critically relevant discoveries that further our understanding of coral resilience."

Now, a year from graduation, Wong is diving deeper into the mechanisms that drive environmental memory within and across coral generations at a molecular level. By using approaches such as metabolomics (the identification and quantification of metabolic by-products), transcriptomics (quantification of gene expression), and epigenetics (features that regulate gene expression), Wong aims to determine the key linkages between metabolism and coral bleaching phenotypes at a cellular level.

Parent-Offspring Conflict

4 Unresolved Issues

4.1 Is Unequal Parental Investment de Facto Evidence of Conflict?

Unequal parental investment is predicted by parent-offspring conflict theory if offspring can move parents off their optimal investment. But is unequal investment de facto evidence of parent-offspring conflict. Almost certainly not. There is a large, expanding literature on why parents may prefer unequal investment in their offspring, up to and including the possibility of infanticide ( Mock and Forbes, 1995 , 1992 ).

In altricial birds or mammals, for example, contemporary offspring though genetic equals are not phenotypic equals. Parents get to make the first move and in doing so can shape the battlefield upon which a conflict takes place ( Alexander, 1974 ). It should not be surprising, therefore, that parents act in ways that are self-serving, sometimes at the expense of their offspring. For example, parents often confer handicaps to some offspring and advantages to others. The most obvious examples are birth or hatching asynchrony where some offspring gain age, size and/or developmental advantages over later hatched brood mates. In birds hatching asynchrony is the cardinal handicap that usually proves decisive in defining the outcome of sibling competition ( Glassey and Forbes, 2002 Forbes, 2011 ). Advantaged ‘core’ offspring (sensu Mock and Forbes, 1995 ) generally secure first access to parentally-provided resources, and enjoy higher survival with lower variation than their ‘marginal’ broodmates ( Forbes et al., 1997 Forbes, 2011 ).

At first glance it would appear that the resulting asymmetric sibling competition that skews parental investment toward core progeny is contrary to the genetic interests of parents ( Mock, 1987 ). But the unequal distribution of resources that results in unequal fitness prospects for the offspring arises by parental fiat, not the outcome of certain offspring winning a parent-offspring conflict. It has become increasingly clear that unequal parental investment and the creation of castes of core and marginal offspring serves parental interests in manifold ways by allowing parents to track uncertain resources ( Lack, 1947 Temme and Charnov, 1987 Kozlowski and Stearns, 1989 Mock and Forbes, 1995 ) to compensate for developmental accidents such as hatching failure or congenital defects ( Cash and Evans, 1986 Anderson, 1990b Forbes, 1990 ) or to facilitate the development of surviving offspring – e.g., by serving as food ( Alexander, 1974 Peters et al., 1999 Perry and Roitberg, 2006 de Vries and Lakes-Harlan, 2007 ). In angiosperms, such unequal treatment of progeny appears to have been canalized into the system of double fertilization where a redundant embryo serves to nourish the other ( Friedman, 1995 ).

Parents may even choreograph paradoxical sibling rivalries where one offspring routinely murders another, the so called Cain-and-Abel battles that occur in some predatory birds ( Gargett, 1978 Cash and Evans, 1986 Anderson, 1989, 1990b ), sharks ( Grant et al., 1983 ) and even plants where some seeds poison others in the same pod ( Ganeshaiah and Shaanker, 1988 ). Such obligate brood reduction would appear antithetical to parental interests as it usually involves the waste of a perfectly good offspring.

But closer scrutiny reveals the opposite. A Nazca booby chick (Sula granti) may push its younger sibling into the searing equatorial sun, resulting in its rapid death due to hyperthermia ( Anderson, 1989 ). The ‘tell’ that this is not a parent-offspring conflict is that this drama unfolds quite literally at the parent’s feet: The parent stands by disinterestedly as the siblicide occurs (for review of parental disinterest in siblicide see Mock and Parker, 1997 ).

The paradox is resolved by the uncomfortable perspective that neither the parent nor the core offspring had any interest in the survival of the marginal offspring. For the parents it was an insurance policy against the hatching failure that often occurs ( Anderson, 1990b ). Nazca boobies are long-lived ( Apanius et al., 2008 ) and raising an extra chick now does not compensate for an elevated rate of parental mortality and lost future reproduction, especially for mothers. Thus once the first (core) chick hatched and demonstrated its viability, the second chick became redundant for both parent and core offspring. Parent and core offspring collaborated in the death of the marginal offspring. The marginal offspring may prefer not to be sacrificed but has little choice in the matter.

4.2 Parents Dodging Conflict: The Evolution of Tamper-proof Mechanisms

Using offspring-provided cures opens the door to offspring manipulation of parental investment , reducing the fitness of parents. A question is this: what is the benefit of using offspring-provided information? Its corollary is: does the benefit exceed the cost of, from the parent’s perspective, supra-optimal investment? The offspring-provided information (e.g., begging displays) could help parents to modulate investment adaptively by providing more for undernourished offspring, or curbing provisioning of overfed progeny.

But differing parent and offspring optima open the door to offspring exaggeration of their needs at a cost to parents. An obvious alternative exists: Ignore offspring cues and base investment decisions on a schedule of parental input – e.g., how much milk has already been provided. If a predictable link exists between offspring phenotype and parental input, then monitoring offspring condition may be superfluous.

Such may be the case in guinea pigs where pups are weaned based on maternal, not offspring cues. A cross-fostering experiment in highly precocial Brazilian guinea pigs (Cavia aperea) revealed that weaning is primarily under maternal control ( Rehling and Trillmich, 2007 ). Swapping older for younger pups did not extend the period of suckling as would be predicted if offspring were, at least in part, in control of weaning. Instead, the duration of lactation appears to be sensitive only to maternal state, as weaning is delayed when mothers are food-restricted ( Laurien-Kehnen and Trillmich, 2003 ). This suggests a physiological program that is insensitive to offspring cues. Such also appears to be the case in marsupials where milk provisioning follows a fixed trajectory ( Tyndale-Biscoe and Renfree, 1987 Findlay and Renfree, 1984 ).

Similarly, Hinde et al. (2010) found that parents – not offspring – controlled provisioning in canaries (Serinus canaria). When confronted with foster broods that begged either more or less than their own brood, parents did not vary their rate of provisioning, and the cross-fostered young grew slower than those on average than those raised by their own parents. When offspring demands and parental supply were mismatched, it was the offspring who paid.

A key question is whether tracking offspring condition pays sufficiently to offset the costs of tracking and in particular the potential for offspring to bias parental investment decisions in their favor. If X grams of input reliably generates Y grams of pup and Z units of fitness, then parents can ignore offspring cues, such as begging or suckling effort. Parker and Macnair (1979) modeled parent-offspring conflict where parents may ignore offspring solicitation in favor of fixed parental investment. They found that a parent-wins evolutionarily stable strategy (ESS) is possible if the costs of ignoring offspring solicitations are small. This result makes intuitive sense. Offspring are expected to exaggerate their needs, reducing parental fitness if parents respond. A better policy may simply be to follow a fixed schedule of parental investment that natural selection can calibrate.

The problem is similar to tracking a variable environment with brood size ( Lack, 1947 Temme and Charnov, 1987 ), usually by creating an optimistic brood size and trimming downward as ecological conditions warrant. Obligate strategies are favored if the tracking mechanism is too costly ( Temme and Charnov, 1987 Forbes and Mock, 1994 ).

A maternal strategy of releasing milk according to a fixed schedule or one dependent only upon maternal condition may be cheaper than incorporating an additional mechanism to monitor offspring state. Mammals nursing pups in a sheltered environment would seem well-suited to inflexible maternal control, as mothers could potentially monitor milk-production precisely. Conversely, such an inflexible mechanism may work less well in an open-cup nest of an altricial bird where a variable thermal environment may make the link between input and offspring condition less predictable due to variable thermoregulatory costs.

The challenge becomes greater in systems of bi-parental care where one parent may not be able to track the input of the other parent. In such cases, parents may need to rely upon offspring to ‘tell’ them about the other parent’s activities. Subdued begging effort may indicate recent feeding by the other parent.

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Older fathers pass on more genetic mutations, study shows

The rising age of fatherhood could be a factor in increased rates of conditions such as schizophrenia and autism, scientists say, after new research suggesting that older fathers pass on more genetic mutations to their children.

A child will normally have 60 new mutations in its genetic sequence (out of a total of more than 3bn DNA letters) passed on from its parents. Despite being a tiny fraction of the sequence, these differences are the root of much of the diversity in the human genomes and, over long periods of time, amount to a significant force in human evolution.

"Most of these mutations are probably neutral," said Kari Stefansson, chief executive of deCODE Genetics in Iceland, who led the latest work, published on Wednesday in Nature.

"Occasionally, they will be deleterious, they will lead to a disease. Once in a blue moon, you will get a mutation that confers a selective advantage. We showed that some of these mutations are in genes that have been indicated in diseases like autism and schizophrenia."

A single-letter mutation in a gene called APP can confer protection against Alzheimer's disease and help people live longer, for example, while a single-letter mutation in the CFTR gene causes cystic fibrosis. Similar single-letter mutations in genes are behind sickle cell anaemia and even colour blindness.

Stefansson said a 40-year-old father was approximately twice as likely to conceive a child that developed autism as a 20-year-old father, although the overall risk remained low. The increase in risk factor for schizophrenia went up by a similar amount. "It's incredibly important to recognise that, even though there is a doubling in risk of a 40-year-old father conceiving a child that develops schizophrenia compared to a 20-year-old, the overall risk is still not above 1%," he said.

Stefansson urged fathers not to worry about having children at an older age. "This has been a fact of life for centuries – nothing has changed with this. This is only giving us an opportunity to quantify the changes that are happening in genomes," he said.

He hoped that the work would, however, shift some of the focus from the increasing age of the mother to the increasing age of the father when it came to concerns about developmental disorders in children.

Alexey Kondrashov of the department of ecology and evolutionary biology at the University of Michigan, in an accompanying analysis for Nature, said: "In humans, as many as 10% of point mutations are deleterious, so [Stefansson's] findings suggest that an average newborn carries six new deleterious mutations. Although most of these mutations will, on their own, have only mild effects, collectively they could have a substantial impact on health."

Stefansson's team studied the mutation rates in 78 Icelandic parent-offspring trios and found that a 20-year-old father transmits, on average, around 25 mutations to his child, whereas a 40-year-old father transmits around 65.

Every additional year of the father's age meant an average of two extra mutations in the child. In comparison, the number of new mutations passed on by the mother was always around 15, regardless of her age.

In Iceland, where the study was carried out, the age of fathers at conception had risen from an average of 27.9 years in 1980 to 33 years in 2011, mainly owing to increased education and the higher use of contraception.

In the UK, the average age of fathers in 2008 was 32.4, up from 31.5 a decade earlier.

Autism spectrum disorders are known to have some genetic triggers and increased rate of mutations from older fathers might be a factor.

Kondrashov said it was unsurprising that disorders of brain function, such as autism, schizophrenia, dyslexia and reduced intelligence, seemed particularly affected by the age of the father. "This is consistent with the fact that more genes are expressed in the brain than in any other organ, meaning that the fraction of new mutations that will affect its functions is the highest."

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Allan Pacey, an andrologist at the University of Sheffield and chairman of the British Fertility Society, said it was a surprise to find that men transmitted a higher number of mutations to their children than women.

Why DNA may matter more than parenting — and what that means for society

By Robert Plomin
Published November 23, 2018 1:00PM (EST)

"Blueprint: How DNA Makes Us Who We Are" by Robert Plomin (MIT Press/Getty/Firstsignal)


Adapted from "Blueprint: How DNA Makes Us Who We Are" by Robert Plomin. Copyright 2018, The MIT Press.

Parents obviously matter tremendously in their children’s lives. They provide the essential physical and psychological ingredients for children’s development. But if genetics provides most of the systematic variance and environmental effects are unsystematic and unstable, this implies that parents don’t make much of a difference in their children’s outcomes beyond the genes they provide at conception. This even includes personality traits that seem especially susceptible to parental influence such as altruism, kindness and conscientiousness. The only exception from hundreds of traits that shows some evidence of shared environmental influence are religious and political beliefs. As a parent, you can make a difference to your child’s beliefs, but even here shared environmental influence accounts for only 20 per cent of the variance.

Furthermore, when differences in parenting correlate with differences in children’s outcomes, the correlation is mostly caused by genetics. These correlations are caused by the nature of nurture rather than nurture. That is, parenting correlates with children’s outcomes for three reasons considered earlier. One reason is that parents and their children are 50 per cent similar genetically. Put crudely, nice parents have nice children because they are all nice genetically. Another reason is that parenting is often a response to, rather than a cause of, children’s genetic propensities. It is awkward to be an affectionate parent to a child who is not a cuddler. Finally, children make their own environments, regardless of their parents. That is, they select, modify and create environments correlated with their genetic propensities. Children who want to do something like play sports or a musical instrument will badger their parents to make it happen.

In essence, the most important thing that parents give to their child is their genes. Many parents will find this hard to accept. As a parent, you feel deep down that you can make a difference in how your children develop. You can help children with their reading and arithmetic. You can help a shy child overcome shyness. Also it seems as if you must be able to make a difference because you are bombarded with child‑rearing books and the media telling you how to do it right and making you anxious about doing it wrong. (These books are, however, useful in providing parenting tips, for example, about how to get children to go to sleep, how to feed fussy children and how to handle issues of discipline.)

But when these best‑selling parenting books promise to deliver developmental outcomes, they are peddling snake oil. Where is the evidence beyond anecdotes that children’s success depends on parents being strict and demanding "tigers" or giving their children grit? There is no evidence that these parenting practices make a difference in children’s development, after controlling for genetics.

This conclusion is also difficult for many of us to accept in relation to our own parents. As you think about your childhood, your parents no doubt loom large, seeming to be the most significant influence in your life. For this reason, it is easy to attribute how we turned out, in good ways and bad, to our parents. If we are happy and confident, we might credit this to our parents’ love and support. Or if we are psychologically damaged, we might blame this on inadequate parenting. However, the implications of genetic research are just as applicable here. These differences in parenting are not correlated with differences in children’s outcomes once you control for genetics. Your parents’ systematic influence on who you are lies with the genes they gave you.

If you are still finding it difficult to accept that parenting is less influential than you thought, it might be useful to review two general caveats about genetics. The first caveat is that genetic research describes what is, not what could be. Parents can make a difference to their child but, on average in the population, parenting differences don’t make a difference in children’s outcomes beyond the genes they share. Parents differ in how much they guide their children in all aspects of development. They differ in how much they push their children’s cognitive development, for example in language and reading. Parents also differ in how much they help or hinder their children’s self‑esteem, self‑confidence, determination, as well as more traditional aspects of personality such as emotionality and sociability. But in the population, these parenting differences don’t make much of a difference in their children’s outcomes once genetics is taken into account. Over half of children’s psychological differences are caused by inherited DNA differences between them. The rest of the differences are largely due to chance experiences. These environmental factors are beyond our control as parents, and yet we don’t even know what these factors are.

The second caveat is that genetic research describes the normal range of variation, genetically and environmentally. Its results do not apply outside this normal range. Severe genetic problems such as single‑gene or chromosomal problems or severe environmental problems such as neglect or abuse can have devastating effects on children’s cognitive and emotional development. But these devastating genetic and environmental events are, fortunately, rare and do not account for much variance in the population.

Again, parents and parenting matter tremendously, even though differences in parenting do not make a difference in children’s psychological development. Parents are the most important relationship in children’s lives. Still, it is important that parents get the message that children are not blobs of clay that can be moulded however they wish. Parents are not carpenters building a child by following a blueprint. They are not even much of a gardener, if that means nurturing and pruning a plant to achieve a certain result. The shocking and profound revelation for parenting from these genetic findings is that parents have little systematic effect on their children’s outcomes, beyond the blueprint that their genes provide.

It is also important for parents to know that, beyond genetics, most of what happens to children involves random experiences over which parents have no control. The good news is that these don’t make much of a difference in the long run. The impact of these experiences is not stable across time. Some children bounce back sooner, some later, after difficult experiences such as parental divorce, moving house and losing friends. They bounce back to their genetic trajectory.

In the tumult of daily life parents mostly respond to genetically driven differences in their children. This is the source of most correlations between parenting and children’s outcomes. We read to children who like us to read to them. If they want to learn to play a musical instrument or play a particular sport, we foster their appetites and aptitudes. We can try to force our dreams on them, for example, that they become a world‑class musician or a star athlete. But we are unlikely to be successful unless we go with the genetic grain. If we go against the grain, we run the risk of damaging our relationship with our children.

Genetics provides an opportunity for thinking about parenting in a different way. Instead of trying to mold children in our image, we can help them find out what they like to do and what they do well. In other words, we can help them become who they are. Remember that your children are 50 per cent similar to you. In general, genetic similarity makes the parent–child relationship go smoothly. If your child is highly active, chances are that you are too, which makes the child’s hyperactivity more acceptable. Even if you both have short fuses, you can at least understand it better if you recognize your genetic propensities and work harder to defuse situations that can trigger anger. It is also useful to keep in mind that our children are 50 per cent different from us and that siblings are 50 per cent different from each other. Each child is their own person genetically. We need to recognize and respect their genetic differences.

Most importantly, parents are neither carpenters nor gardeners. Parenting is not a means to an end. It is a relationship, one of the longest lasting in our lives. Just as with our partner and friends, our relationship with our children should be based on being with them, not trying to change them.

I hope this is a liberating message, one that should relieve parents of the anxiety and guilt piled on them by parent‑blaming theories of socialization and how‑to parenting books. These theories and books can scare us into thinking that one wrong move can ruin a child forever. I hope it frees parents from the illusion that a child’s future success depends on how hard they push them.

Instead, parents should relax and enjoy their relationship with their children without feeling a need to mold them. Part of this enjoyment is in watching your children become who they are.

Schools matter, but they don’ t make a difference

The same principles apply to education. Schools matter in that they teach basic skills such as literacy and numeracy and they dispense fundamental information about history, science, math, and culture. That is why basic education is compulsory in most countries around the world. Schools also matter because children spend half of their childhood in school.

But our focus is on individual differences. Children differ a lot in how well they do at school. How much do differences in children’s school achievement depend on which school they go to? The answer is not much. This conclusion follows from direct analyses of the effect of schools on differences in students’ achievement and is especially true when we control for genetic effects.

In the UK "league tables" rank schools by their average differences in tested achievement. In addition, rigorous government inspections of schools rank them by their quality of teaching and the support they give their pupils. Schools differ on average for both indices, but the question here is how much variance in student achievement is explained by schooling. These indices lead parents to worry about sending their children to the best schools, based on the assumption that schools make a big difference in how much children achieve.

In fact, differences in schools do not make much of a difference in children’s achievement. Most striking are results using the intensive and expensive periodic ratings of school quality, including teacher quality and the atmosphere of the school, based on visits to each school every three years or so by a team of assessors from the UK Office for Standards in Education (Ofsted). We correlated these Ofsted ratings of children’s secondary schools with the children’s achievement assessed on the General Certification of Secondary Education (GCSE) tests administered to UK students in state‑supported schools at the age of sixteen. The Ofsted ratings of school quality explained less than 2 per cent of the variance in GCSE scores after correcting for students’ achievement in primary school. That is, children’s GCSE scores scarcely differ as a function of their schools’ Ofsted rating of quality. This does not mean that the quality of teaching and support offered by schools is unimportant. It matters a lot for the quality of life of students, but it doesn’t make a difference in their educational achievement.

The conclusion that schools do not make much difference in children’s achievement seems surprising, given the media attention on average differences between schools in student performance. This reflects the confusion between average differences and individual differences. Average differences between schools in the league tables mask a wide range of individual differences within schools, meaning that there is considerable overlap in the range of performance between children in the best and worst schools. In other words, some children in the worst schools outperform most children in the best schools. The biggest average difference in achievement is between selective and non‑selective schools.

Inherited DNA differences account for more than half of the differences between children in their school achievement. Genetics is by far the major source of individual differences in school achievement, even though genetics is rarely mentioned in relation to education.

Environmental factors account for the rest of the variance in school achievement, but most of these environmental differences are not the result of systematic and stable effects of schooling. Environmental influence shared by children attending the same schools as well as growing up in the same family accounts for only 20 per cent of the variance of achievement in the school years and less than 10 per cent of academic performance at university.

The other crucial finding about the environment is the nature of nurture. What look like environmental effects are reflections of genetic differences. In relation to education, what looks like environmental effects of schools on children’s achievement are actually genetic effects. Examples include the correlation between student achievement and types of school and the correlation between parent and offspring educational achievement. Both correlations are usually interpreted as being caused environmentally but both are substantially mediated by genetics.

No specific policy implications necessarily follow from finding that inherited DNA differences are by far the most important source of individual differences in school achievement and that schools make so little difference. Similar to the message for parents, genetic research suggests that teachers are not carpenters or gardeners in the sense of changing children’s school performance. Rather than frenetic teaching in an attempt to make pupils pass the tests that will improve their standing in league tables, schools should be supportive places for children to spend more than a decade of their lives, places where they can learn basic skills like literacy and numeracy but also learn to enjoy learning. To paraphrase John Dewey, the major American educational reformer of twentieth century, education is not just preparation for life – education is a big chunk of life itself.

Life experiences matter, but they don’ t make a difference

Genetic research has far‑reaching implications not just for how we think about child‑rearing and schools but how we think about our own adult lives. Genetics is the major systematic influence in our lives, increasingly so as we get older. Therefore, genetics is a big part of understanding who we are. Our experiences matter a lot – our relationships with partners, children and friends, our occupations and interests. These experiences make life worth living and give it meaning. Relationships can also change our behavior, such as helping us to stop smoking or lose weight. They can affect our lifestyle by encouraging us to exercise, play sports and go to cultural events. But they don’t change who we are psychologically – our personality, our mental health and our cognitive abilities. Life experiences matter and can affect us profoundly, but they don’t make a difference in terms of who we are.

This conclusion follows from the same suite of genetic findings that we have applied to parenting and schooling: significant and substantial genetic influence, the nature of nurture and the importance of non‑shared environment.

Individual differences in stressful life events were among the first environmental measures for which genetic influence was found. Most research on life events used self‑report measures of stressful events and their effects. However, we saw that even objectively measured events such as divorce show genetic influence. Parental divorce is the best predictor of children’s divorce, but this correlation, easily interpreted as environmental, is entirely due to genetics. Quality of social support is another major aspect of life experiences that has been assumed to be a source of environmental influence but is in fact substantially caused by genetic differences.

Finding genetic influence on individual differences in ‘environmental’ measures led to research that showed that genetics accounts for about half of the correlations between life experiences and psychological traits, such as the correlation between perceptions of life events and depression. This is another example of the nature of nurture.

The point is that life experiences are not just events that happen haplessly to us as passive bystanders. With all our genetically rich psychological differences, we differ in our propensities to experience life events and social support. The nature of nurture suggests a new model of experience in which we actively perceive, interpret, select, modify and create experiences correlated with our genetic propensities.

The importance of non‑shared environment has major implications as well for understanding why life experiences don’t make a difference psychologically. The heritability of life experiences is about 25 per cent, which means that most of the individual differences in life experiences are environmental in origin. But these environmental influences are not shared by our siblings, even if our sibling is our identical twin. Our parents cannot take much credit or blame for how we turned out, other than via the genes they gave us. No one can take credit or blame because these non‑shared environmental influences are unsystematic and unstable. Beyond the systematic and stable force of genetics, good and bad things just happen. As mentioned earlier in relation to parenting, the good news is that these random experiences don’t matter much in the long run because their impact is not long‑lasting. We eventually rebound to our genetic trajectory. To the extent that our experiences appear shared, systematic and stable, they reflect our genetic propensities. These correlations are caused genetically, not environmentally.

In summary, parents matter, schools matter and life experiences matter, but they don’t make a difference in shaping who we are. DNA is the only thing that makes a substantial systematic difference, accounting for 50 per cent of the variance in psychological traits. The rest comes down to chance environmental experiences that do not have long‑term effects.

Many psychologists will be aghast at this bold conclusion. Karl Popper said that the first commandment of science is that theories are not merely testable but falsifiable. Falsifying this conclusion is straightforward: Demonstrate that ‘environmental’ factors such as parenting, schooling and life experiences make a difference environmentally after controlling for genetic influence. Anecdotes are not enough, and it’s not enough to show a statistically significant effect – the issue is whether these things explain more than 1 or 2 per cent of the variance. I am not worried about the conclusion being falsified, because there is a century of research behind it.

One general message that should emerge from these discoveries is tolerance for others – and for ourselves. Rather than blaming other people and ourselves for being depressed, slow to learn or overweight, we should recognize and respect the huge impact of genetics on individual differences. Genetics, not lack of willpower, makes some people more prone to problems such as depression, learning disabilities and obesity. Genetics also makes it harder for some people to mitigate their problems. Success and failure – and credit and blame – in overcoming problems should be calibrated relative to genetic strengths and weaknesses.

Going even further out on this limb, I’d argue that understanding the importance of genetics and the random nature of environmental influences could lead to greater acceptance and even enjoyment of who we are genetically. Rather than striving for an ideal self that sits on an impossibly tall pedestal, it might be worth trying to look for your genetic self and to feel comfortable in your own skin. Moreover, as we have seen, with age, as genetic influence increases, the more we become who we are.

By pointing out that most of the systematic variance in life is caused by inherited DNA differences I do not mean to imply that people should not try to work on any of their shortcomings or not try to improve certain aspects of themselves. Heritability describes what is but does not predict what could be, as I have emphasized several times. High heritability of weight does not mean there is nothing you can do about your weight. Nor does heritability mean that we must succumb to our genetic propensities to depression, learning disabilities or alcohol abuse. Genes are not destiny. You can change. But heritability means that some people are more vulnerable to these problems and also find it more difficult to overcome them.

"If at first you don’t succeed, try, try again" (Thomas Palmer) "Be all that you can be" (US Army) "Anyone can grow up to be President" (Americans) – throughout our lives we are bombarded with inspirational aphorisms like these, from childhood songs like the itsy‑bitsy spider climbing up the water spout and stories like "The Little Engine that Could" to adult fables like Robert the Bruce watching a spider repeatedly trying to build a web, as well as many autobiographies, novels and films about overcoming the odds. The barrage also comes from pop‑psychology books whose message is that all you need to succeed is some panacea, such as the power of positive thinking or a growth mindset or grit or 10,000 hours of practice.

Anyone who is influenced by these maxims should understand that, to the contrary, genetics is the main systematic force in life. Again, this is not to say that genes are destiny. It just seems more sensible, when possible, to go with the genetic flow rather than trying to swim upstream. As W. C. Fields said, "If at first you don’t succeed, try, try again. Then quit. There’s no use being a damn fool about it."

Adapted from "Blueprint: How DNA Makes Us Who We Are" by Robert Plomin. Copyright 2018, The MIT Press.

Difference Between DNA and Genes

The terms gene and DNA are often used to mean the same. However, in reality, they stand for very different things. So, next time you want to blame your baldness on your father and don’t know whether to berate your genes or your DNA, take a look at the differences below:

DNA stands for deoxyribonucleic acid. This is the chain of ‘links’ that determines how the different cells in your body will function. Each of these links is called a nucleotide. DNA basically contains two copies of 23 chromosomes each, one from the mother and one from the father of the person. Only some of these complex cells carry the ‘genetic information for your genes. These are the parts that decide what you basically inherit from your parents. This makes genes only a subset of the DNA.

Your genes define the fundamental traits you will inherit from your parents. They are parts of the DNA that determine how the cells are going to live and function. They are special colonies of nucleotides that decide how proteins are going to carry on the process of building and reproducing in your body. All living things depend on their genes to determine how they are going to develop in their lives and how they, in turn are going to pass on their genetic traits to their offspring.

For instance, if you thought about the human body as a book that contained only DNA, the genes would be the chapter containing instructions on how to make proteins and assist in cell production. The other chapters may contain other details like where the cells should start producing new proteins etc.

The DNA is like an instruction booklet that determines the traits you are likely to get. The entire DNA in a human body is packaged in the form of chromosomes. Each of these chromosomes has definite characters that will determine a particular trait. This includes such details like your hair color and the color of your eyes. Each of these chapters that contain the codes for a particular trait is known as a gene. So, if you are confused, just think about the gene as a small piece of the total DNA that holds information about a particular trait you have.

The study of genetics has gained widespread acclaim in recent times. However, it was only with the discovery of the DNA that a scientific basis for the genes we inherit was established.

Both DNA and genes are the most basic building blocks of your body. They determine how your cells are going to behave throughout your life. Now you know who to thank for those brains!

1. Genes are a part of the DNA.
2. Genes determine the traits you will inherit from your parents, DNA determines a lot more.
3. Genes have been studied for a long time now. The study of DNA is a relatively recent development.

Multiple Choice Questions
Single Correct Answer Type

1. A few statements describing certain features of reproduction are given below
i. Gametic fusion takes place
ii. Transfer of genetic material takes place
iii. Reduction division takes place
iv. Progeny have some resemblance with parents
Select the options that are true for both asexual and sexual reproduction from the options given below:
(a) i and ii (b) ii and iii
(c) ii and iv (d) i and iii
Answer. (c) Transfer of genetic material and progeny have some resemblance with parents are the phenomenon common in’both asexual and sexual reproduction while gametic fusion and reduction division takes place in sexual reproduction only.

2. The term ‘ clone ’ cannot be applied to offspring formed by sexual reproduction because
(a) Offspring do not possess exact copies of parental DNA
(b) DNA of only one parent is copied and passed on to the offspring
(c) Offspring are formed at different times
(d) DNA of parent and offspring are completely different
Answer. (a)
• In asexual reproduction, a single individual (parent) is capable of producing offspring which are not only identical to one another but are also exact copies of their parent. The term clone is used to describe such morphologically and genetically similar individuals.
• In sexual reproduction because of the fusion of male and female gametes (either by same individual or by different individual of the opposite sex), sexual reproduction results in offspring that are not identical to the parents or amongst themselves.

3. Amoeba and Yeast reproduce asexually by fission and budding respectively, because they are
(a) Microscopic organisms
(b) Heterotrophic organisms
(c) Unicellular organisms
(d) Uninucleate organisms
Answer. (c) Many single-celled organisms reproduce by binary fission (e.g., Amoeba, Paramecium), where a cell divides into two halves and each rapidly grows into an adult.
In yeast, the division is unequal and small buds are produced that remain attached initially to the parent cell which eventually gets separated and mature into new yeast organism (cells). Budding is also found in Hydra.

4. A few statements with regard to sexual reproduction are given below
i. Sexual reproduction does not always require two individuals
ii. Sexual reproduction generally involves gametic fusion
iii. Meiosis never occurs during sexual reproduction
iv. External fertilisation is a rule during sexual reproduction
Choose the correct statements from the options below:
(a) i and iv , (b) i and ii
(c) ii and iii (d) i and iv
Answer. (b)
• Sexual reproduction requires male and female gametes (either by same individual or by different individual of the opposite sex).
• Sexual reproduction generally involves gametic fusion.
• Meiosis occurs during sexual reproduction in dipoloid organisms.
• External fertilisation is not a rule during sexual reproduction, internal fertilization also takes place

5. A multicellular, filamentous alga exhibits a type of sexual life cycle in which the meiotic division occurs after the formation of zygote. The adult filament of this alga has
(a) Haploid vegetative cells and diploid gametangia
(b) Diploid vegetative cells and diploid gametangia
(c) Diploid vegetative cells and haploid gametangia
(d) Haploid vegetative cells and haploid gametangia
Answer. (d) Adult filament of a multicellular, filamentous alga have haplontic life cycle in which the meiotic division occurs after the formation of zygote. So, the filament of this alga have haploid vegetative cells and haploid gametangia.

6. The male gametes of rice plant have 12 chromosomes in their nucleus. The chromosome number in the female gamete, zygote and the cells of the seedling will be, respectively,
(a) 12,24,12 . (b) 24,12,12
(c) 12,24,24 (d) 24,12,24
Answer. (c) Gametophytic structure (n) of rice plant contain 12 chromosomes and sporophytic structure (2n) of rice contain 24 chromosomes.
Female gamete (n) =12,
Zygote (2n) = 24,
The cells of the seedling (2n) = 24.

7. Given below are a few statements related to external fertilization. Choose the correct statements.
i. The male and female gametes are formed and released simultaneously.
ii. Only a few gametes are released into the medium.
iii. Water is the medium in a majority of organisms exhibiting external fertilization.
iv. Offspring formed as a result of external fertilization have better chance of survival than those formed inside an organism.
(a) iii and iv (b) i and iii
(c) ii and iv (d) i and iv .
Answer. (b) In most aquatic organisms, such as a majority of algae and fishes as well as amphibians, syngamy occurs in the external medium (water), i.e., outside the body of the organism. This type of gametic fusion is called external fertilisation. Organisms exhibiting external fertilisation show great synchrony between the sexes and release a number of gametes into the surrounding medium (water) in order to enhance the chances of syngamy. This happens in the bony fishes and frogs where a large number of offspring are produced. A major disadvantage is that the offspring are extremely vulnerable to predators threatening their survival up to adulthood.

8. The statements given below describe certain features that are observed in the pistil of flowers.
i. Pistil may have many carpels
ii. Each carpel may have more than one ovule
iii. Each carpel has only one ovule
iv. Pistil have only one carpel
Choose the statements that are true from the options below:
(a) i and ii (b) i and iii
(c) ii and iv (d) iii and iv
Answer. (a)
• Pistil may have many carpels (multicapillary pistil like Papaver)
• Each carpel may have more than one ovule (like Watermelon,.Papaya etc.)

9. Which of the following situations correctly describe the similarity between an angiosperm egg and a human egg?
i. Eggs of both are formed only once in a lifetime
ii. Both the angiosperm egg and human egg are stationary
iii. Both the angiosperm egg and human egg are motile transported
iv. Syngamy in both results in the formation of zygote
Choose the correct answer from the options given below:
(a) ii and iv (b) iv only
(c) iii and iv (d) i and iv
Answer. (b) Syngamy in both results in the formation of zygote is similarity between an angiosperm egg and a human egg.

10. Appearance of vegetative propagules from the nodes of plants such as sugarcane and ginger is mainly because
(a) Nodes are shorter than intemodes
(b) Nodes have meristematic cells
(c) Nodes are located near the soil
(d) Nodes have non-photosynthetic cells
Answer. (b) Appearance of vegetative propagules from the nodes of plants such as sugarcane and ginger is mainly because nodes have meristematic cells. Examples of vegetative propagules: (i) Leaf buds of bryophyllum, (ii) Eyes of potato, (iii) Bulbifof Agave, (iv) Offset of water hyacinth, (v) Rhizome of ginger.

11. Which of the following statements, support the view that elaborate sexual reproductive process appeared much later in the organic evolution?
i. Lower groups of organisms have simpler body design
ii. Asexual reproduction is common in lower groups
iii. Asexual reproduction is common in higher groups of organisms
iv. The high incidence of sexual reproduction in angiosperms and vertebrates
Choose the correct answer from the options given below:
(a) i, ii and iii (b) i, iii and iv
(c) i, ii and iv (d) ii, iii and iv
Answer. (c) Elaborate sexual reproductive process appeared much later in the organic evolution because of
• Lower groups of organisms have simpler body design.
• Asexual reproduction is common in lower groups of organisms.
• High incidence of sexual reproduction in angiosperms and vertebrates.

12. Offspring formed by sexual reproduction exhibit more variation than those formed by asexual reproduction because
(a) Sexual reproduction is a lengthy process
(b) Gametes of parents have qualitatively different genetic composition
(c) Genetic material comes from parents of two different species
(d) Greater amount of DNA is involved in sexual reproduction
Ans. (b)
• Offspring formed by sexual reproduction exhibit more variation than those formed by asexual reproduction because gametes of parents have qualitatively different genetic composition.
• In asexual reproduction due to involvement of only one parent, so there is no chance of variation.

13. Choose the correct statement from amongst the following:
(a) Dioecious (hermaphrodite) organisms are seen only in animals.
(b) Dioecious organisms are seen only in plants.
(c) Dioecious organisms are seen in both plants and animals.
(d) Dioecious organisms are seen only in vertebrates.
Answer. (c) Dioecious organisms are seen in both plants (like papaya) and animals (like cockroach).

14. There is no natural death in single celled organisms like Amoeba and bacteria because
(a) They cannot reproduce sexually
(b) They reproduce by binary fission
(c) Parental body is distributed among the offspring
(d) They are microscopic
Answer. (c) There is no natural death in single celled organisms like Amoeba and bacteria because the parental body is distributed among the offspring.

15. There are various types of reproduction. The type of reproduction adopted by an organism depends on
(a) The habitat and morphology of the organism
(b) Morphology of the organism
(c) Morphology and physiology of the organism
(d) The organism’s habitat, physiology and genetic make up
Answer. (d) The organism’s habitat, its internal physiology and several other factors (genetic make up) are collectively responsible for how it reproduces. When offspring is produced by a single parent with or without the involvement of gamete formation, the reproduction is asexual.

16. Identify the incorrect statement.
(a) In asexual reproduction, the offspring produced are morphologically and genetically identical to the parent.
(b) Zoospores are sexual reproductive structures.
(c) In asexual reproduction, a single parent produces offspring with or without the formation of gametes.
(d) Conidia are asexual structures in Penicillium.
Answer. (b) Zoospores are asexual reproductive structures.

17.Which of the following is a post-fertilisation event in flowering plants?
(a) Transfer of pollen grains
(b) Embryo development
(c) Formation of flower
(d) Formation of pollen grains
Answer. (b)

18. The number of chromosomes in the shoot tip cells of a maize plant is 20. The number of chromosomes in the micro spore mother cells of the same plant shall be
(a) 20 (b) 10 (c) 40 (d) 15
Answer. (a) Shoot tip cells of a maize plant is a sporophytic structure (2n) and microspore mother cells of maize plant is also a sporophytic structure (2n). So, microspore mother cells (MMC) contain 20 chromosomes.

Very Short Answer Type Questions
1. Mention two inherent characteristics of Amoeba and yeast that enable them to reproduce asexually.
Answer. a. They are unicellular organisms.
b. They have a very simple body structure.

2. Why do we refer to’offspring formed by asexual method of reproduction as clones?
Answer. Offspring formed by asexual reproduction are called clones because they are morphologically and genetically similar to the parent.

3. Although potato tuber is an underground part, it is considered as a stem. Give two reasons.
Answer. a. The tuber has nodes and intemodes (as stem),
b. Leafy shoots appear from the nodes.

4. Between an annual and a perennial plant, which one has a shorter juvenile phase? Give one reason.
Answer. An annual has a shorter juvenile phase. Since its entire life cycle has to be completed in one growing season, its juvenile phase is shorter.

5. Rearrange the following events of sexual reproduction in the sequence in which they occur in a flowering plant: embryogenesis, fertilisation, gametogenesis, pollination.
Answer. Gametogenesis, Pollination, Fertilisation, Embryogenesis

6. The probability of fruit set in a self-pollinated bisexual flower of a plant is far greater than a dioecious plant. Explain.
Answer. There is assured fruit set in self pollinated bisexual flower even in the absence of pollinators. In dioecious plants, there is male and female flowers present on different plants, so external pollinating agent is required for pollination.

7. Is the presence of large number of chromosomes in an organism a hindrance to sexual reproduction? Justify your answer by giving suitable reasons.
Answer. Presence of large number of chromosomes in an organism is not a hindrance to sexual reproduction. Butterfly has 380 chromosomes but it can reproduce sexually.

8. Is there a relationship between the size of an organism and its life span? Give two examples in support of your answer.
Answer. Life spans of organisms are not necessarily correlated with their sizes. The sizes of crows and parrots are not very different yet their life spans show a wide difference. Live span of crow is 15 year and of parrot is 140 years. A mango tree has a much shorter life span as compared to a peepal tree.

9. In the figure given below, the plant bears two different types of flowers marked ‘A’ and ‘B Identify the types of flowers and state the type of pollination that will occur in them.

Answer. ‘A’ is chasmogamous flower while ‘B’ is cleistogamous flower. A bisexual flower which normally open is called chasmogamous flower. Cleistogamous flowers do not open at all.
Cleistogamous flowers are invariably autogamous as there is no chance of cross-pollen landing on the stigma.
In a normal flower which opens and exposes the anthers and stigma complete autogamy is rather rare. Chasmogamous flower may show autogamy, geitonogamy or xenogamy.

10. Give reasons as to why cell division cannot be a type of reproduction in multicellular organisms.
Answer. Cell division cannot be a type of reproduction in multicellular organisms because cell division only increases the number of cells in an organism which leads to the growth of body.

11. In the figure given below, mark the ovule and pericarp.


12. Why do gametes produced in large numbers in organisms exhibit external fertilisation?
Answer. Organisms exhibiting external fertilisation release a number of gametes into the surrounding medium (water) in order to enhance the chances of syngamy because there are few’ chances of fusion between male and female gametes.

13. Which of the followings are monoecious and dioecious organisms?
a. Earthworm ——————–
b. Chara ——————–
c. Marchantia ——————-
d. Cockroach ——————–
Answer. a. Earthworm—Monoecious
b. Chara—Monoecious
c. Marchantia—Dioecious
d. Cockroach—Dioecious

14. Match the organisms given in Column ‘A’ with the vegetative propagules given in column ‘B’.

Answer. Bryophyllum—leaf buds Agave—bulbils Potato—eyes
Water hyacinth—offset

15. What do the following parts of a flower develop into after fertilisation?
a. Ovary
b. Ovules
Answer. a. Ovary—Fruit
b. Ovules—Seeds

Short Answer Type Questions
1. In haploid organisms that undergo sexual reproduction, name the stage in the life cycle when meiosis occurs. Give reasons for your answer.
Answer. Meiosis takes place during its post-zygotic stage. Since the organism is haploid, meiosis cannot occur during gametogenesis.

2. The number of taxa exhibiting asexual reproduction is drastically reduced in higher plants (angiosperms) and higher animals (vertebrates) as compared with lower groups of plants and animals. Analyse the possible reasons for this situation.
Answer. Both angiosperms and vertebrates have a more complex structural organisation. They have evolved very efficient mechanism of sexual reproduction. Since asexual reproduction does not create new genetic pools in the offspring and consequently hampers their adaptability to external conditions, these groups have resorted to reproduction by the sexual method.

3. Honeybees produce their young ones only by sexual reproduction. Inspite of this, in a colony of bees we find both haploid and diploid individuals. Name the haploid and diploid individuals in the colony and analyse the reasons behind their formation.
• The colony of honey bees has three types of members: (i) Diploid queen are fertile females, (ii) Worker bees are sterile females and (iii) Drones are haploid males.
• An offspring formed from the union of a sperm and an egg develops as a female (queen or worker), and an unfertilized egg develops as a male (drone) by means of parthenogenesis. This means that the males have half the number of chromosomes than that of a female.

4. With which type of reproduction do we associate the reduction division? Analyse the reasons for it.
Answer. Reduction division (meiosis) is associated with sexual reproduction. The reasons for this are:
a. Since sexual reproduction involves the fusion of two types of gametes (male and female), they must have haploid number of chromosomes.
b. The cell (meiocyte) which gives rise to gametes often has diploid number of chromosomes and it is only by reducing the number by half that we can get haploid gametes.
c. Reduction division also ensures maintenance of constancy of chromosome number from generation to generation.

5. Is it possible to consider vegetative propagation observed in certain plants like Bryophyllum, water hyacinth, ginger etc., as a type of asexual reproduction? Give two/three reasons.
Answer. Vegetative propagation is considered as a type of asexual reproduction because
(i) This is uniparental.
(ii) Clone formation takes place.
(iii) There is no fertilisation.

6. ‘Fertilisation is not an obligatory event for fruit production in certains plants’. Explain the statement.
Answer. Yes, it is observed in parthenocarpic fruits. The ‘seedless fruits’ that are available in the market such as pomegranate, grapes etc. are in fact good examples. Flowers of these plants are sprayed by a growth hormone that induces fruit development even though fertilisation has not occurred. The ovules of such fruits, however, fail to develop into seeds.

7. In a developing embryo, analyse the consequences if cell divisions are not followed by cell differentiation.
Answer. During embryogenesis, zygote undergoes cell-division (mitosis) and cell differentiation. While cell divisions increase the number of cells in the developing embryo Cell differentiation helps groups of cells to undergo certain modifications to form specialised tissues and organs to form an organism.
If cell divisions are not followed by cell differentiation then there will be no formation of tissues or organs, so a new organisms cannot be formed.

8. List the changes observed in an angiosperm flower subsequent to pollination and fertilisation.
Answer. Post-fertilisation modifications

9. Suggest a possible explanation why the seeds in a pea pod are arranged in a row, whereas those in tomato are scattered in the juicy pulp.
Answer. In a fruit, seed arrangement depends on type of placentation. Pea and tomato shows different placentation. Pea shows marginal placentation while tomato shows axile placentation.

10. Draw the sketches of a zoospore and a conidium. Mention two dissimilarities between them and alt least one feature common to both structures.

11. Justify the statement ‘Vegetative reproduction is also a type of asexual reproduction’.
Answer. Vegetative propagation is also a type of asexual reproduction because
(i) This is uniparental.
(ii) Clone formation takes place.
(iii) There is no fertilisation.
(iv) There is no gamete formation.

Long Answer Type Question
1. Enumerate the differences between asexual and sexual reproduction. Describe the types of asexual reproduction exhibited by unicellular organisms.

The types of asexual reproduction exhibited by unicellular organisms:
• Many single-celled organisms reproduce by binary fission (e.g., Amoeba, Paramecium), where a cell divides into two halves and each rapidly grows into an adult.
• In yeast, the division is unequal and small buds are produced that remain attached initially to the parent cell which eventually gets separated and mature into new yeast organism (cells).

2. Do all the gametes formed from a parent organism have the same genetic composition (identical DNA copies of the parental genome)? Analyse the situation with the background of gametogenesis and provide or give suitable explanation.
Answer. The gametes of a parent do not have the same genetic composition because they do not have identical copies of DNA. In the pachytene and diplotene stages of meiosis-I, the phenomenon of crossing over and chiasma formation take place between homologous chromosomes. This shifts segments of DNA from one chromatid to another (homologous chromosomes) in a random manner resulting in several new combinations of DNA sequences. As a result, when meiotic division is completed, gametes possess DNA with varying degree of variations.

3. Although sexual reproduction is a long drawn, energy-intensive complex form of reproduction, many groups of organisms in Kingdom Animalia and Plantae prefer this mode of reproduction. Give at least three reasons for this.
Answer. a. Sexual reproduction brings about variation in the offspring.
b. Since gamete formation is preceded by meiosis, genetic recombination occurring during crossing over (meiosis-I), leads to a great deal of variation in the DNA of gametes.
c. The organism has better chances survival in a changing environment.

4. Differentiate between (a) oestrus arid menstrual cycles (b) ovipary and vivipary. Cite an example for each type.
Answer. Differences between oestrus and menstrual cycles

5. Rose plants produce large, attractive bisexual flowers but they seldom produce Suits. On the other hand a tomato plant produces plenty of fruits though they have small flowers. Analyse the reasons Tor failure of fruit formation in rose.
Answer. Failure of fruit formation in rose may be due to several reasons. Some of the likely reasons are
a. Rose plants may not produce viable pollen.
b. Rose plants may not have functional egg.
c. Rose plants may have abortive ovules.
d. Being hybrids, the meiotic process may be abnormal resulting in non-viable gametes. ‘
e. There may be self-incompatibility.
f. There may be internal barriers for pollen tube growth and/or fertilisation.

Transgenerational effects of parental light environment on progeny competitive performance and lifetime fitness

Plant and animal parents may respond to environmental conditions such as resource stress by altering traits of their offspring via heritable non-genetic effects. While such transgenerational plasticity can result in progeny phenotypes that are functionally pre-adapted to the inducing environment, it is unclear whether such parental effects measurably enhance the adult competitive success and lifetime reproductive output of progeny, and whether they may also adversely affect fitness if offspring encounter contrasting conditions. In glasshouse experiments with inbred genotypes of the annual plant Polygonum persicaria, we tested the effects of parental shade versus sun on (a) competitive performance of progeny in shade, and (b) lifetime reproductive fitness of progeny in three contrasting treatments. Shaded parents produced offspring with increased fitness in shade despite competition, as well as greater competitive impact on plant neighbours. Inherited effects of parental light conditions also significantly altered lifetime fitness: parental shade increased reproductive output for progeny in neighbour and understorey shade, but decreased fitness for progeny in sunny, dry conditions. Along with these substantial adaptive and maladaptive transgenerational effects, results show complex interactions between genotypes, parent environment and progeny conditions that underscore the role of environmental variability and change in shaping future adaptive potential.

This article is part of the theme issue ‘The role of plasticity in phenotypic adaptation to rapid environmental change’.

1. Introduction

It is increasingly recognized that even the relatively rapid process of contemporary selective evolution [1] may be too slow to permit organisms to adaptively keep pace with rapidly changing environments [2–6], and that individual plasticity may provide a critical source of adaptive adjustment over very short timescales (e.g. [7,8] reviewed in [9–12]). However, the adaptive effectiveness of plastic response may be limited by the time required for the developing individual to perceive its environment and initiate appropriate phenotypic adjustments [13–16]. This time lag is eliminated (in all but the inducing generation) in plant and animal taxa that express adaptive transgenerational plasticity, whereby individuals respond to specific environmental states by modifying traits of their progeny in ways that preadapt them to those same conditions ([17–28] in plants and [29–33] in animals). Because this mode of phenotypic change can be induced after just one generation in a new environment, and may be expressed in many offspring at once in that environment, transgenerational effects may enhance a population's persistence in the face of variable or rapidly changing conditions [34–38]. Note that these inherited changes to progeny phenotypes are not simply ‘silver spoon’ effects [39], in which maternal plants and animals in favourable conditions produce higher quality, more well-provisioned progeny that have universally enhanced growth, competitive success and fecundity (reviewed in [40–46]). These positive effects of favourable maternal conditions are unlikely to provide adaptation to anthropogenically changed environments, which generally entail abiotic or biotic stresses. Rather, plastic transgenerational effects may provide such ‘adaptive rescue’, because they consist of changes to offspring made by parents in response to particular—often stressful—environments that confer the specific traits necessary for maximizing fitness in those environments.

Not surprisingly, this remarkable aspect of plasticity has excited a great deal of interest as a potential source of rapid adaptive change in natural populations facing new challenges. Yet two key questions remain to be answered in order to evaluate its potential impact in natural systems [47,48]. First, do transgenerational effects of parental environment significantly alter the realized success of offspring? Among published studies that show beneficial transgenerational effects of parental stresses on progeny development in similar conditions (see references above), very few have directly tested effects on either key ecological interactions such as competition [49] or lifetime reproductive fitness [50]. Apart from a small number of cases that document positive effects on juvenile survival [23,26,31,51] or reproductive output (to date, in arthropods only: [52–54]), the vast majority of such studies in both animals and plants focus on progeny size traits such as rosette diameter [55], larval size [56], or biomass [24,27,57], or on the size or number of defensive structures [29,58]. While such growth traits may influence reproductive output in various circumstances, direct measures of fitness impact are essential to assess the adaptive significance of transgenerational effects.

Second, does the direction of such fitness effects (positive or negative) vary depending on the environment? The ecological and fitness consequences of inherited plastic modifications (unlike ‘silver spoon’ effects) will likely be context-dependent: if parent individuals respond to an environmental challenge by producing progeny able to withstand that particular challenge this phenotype may comprise an adaptive mismatch in contrasting conditions with different phenotypic optima [50,59–61]. In other words, inherited effects of parental environments on development may be maladaptive rather than adaptive, if progeny individuals encounter dissimilar rather than similar environmental conditions. If this is the case, the fitness consequences of transgenerational effects will depend crucially on the interplay of spatial and temporal environmental variability with both dispersal and seed (or egg) longevity. Testing for context-dependent fitness impacts requires transgenerational studies designed to include ecologically realistic alternative offspring environments that can reveal potentially maladaptive effects (e.g. [23,24,54,62]).

Rigorous tests for adaptive consequences of transgenerational effects require a two-step experimental design that isolates progeny variation due to parental environment from variation due to parental genotype [38,50]: (i) replicate parents of each experimental genotype must be raised in two (or more) treatments to generate progeny differing only in parental environment, and (ii) these sets of progeny must be tested factorially in two (or more) offspring treatments these treatments need not be identical to the parent environments, but they must have different adaptive optima. Clearly, such tests will be most meaningful if they are carried out with naturally evolved systems, and in ecologically relevant alternative environmental states in addition, an accurate measurement of lifetime fitness is essential. Here, we present a study using naturally evolved (field-based) genotypes of Polygonum persicaria, a widespread herbaceous plant of diverse temperate habitats. This species offers three key experimental advantages: first, it has a mixed breeding system (i.e. populations undergo both outcrossing and self-fertilization [63]), so genotypes are diverse, as in most systems, yet can be intensively inbred to produce isogenic replicate parents [64]. Second, P. persicaria is an obligate annual, so total reproductive output (i.e. fitness) can be directly measured. Finally, the range and variability of major environmental factors have been characterized for natural source populations [65], providing a robust context for the design of experimental treatments [15].

We investigated transgenerational effects of parental environment on progeny competitive performance and lifetime fitness, in response to a key environmental variable for plants: light. Light conditions vary in all natural plant habitats [66], as incident solar radiation is mediated in both quantity and spectral quality by canopy and neighbour shade [67]. Because different phenotypes are required for maximizing growth and competitive success in shaded versus full-sun conditions ([66,68,69], and references therein), any transgenerational effects of parental light environment could potentially influence progeny fitness in alternative conditions. Within- and among-site patterns of light variation are expected to change in future climatic and atmospheric conditions, reflecting denser canopies in some systems [66] and sunnier, drier conditions in others [70–73]. Moreover, increased variability in temperature and precipitation [74–76] may lead to greater year-to-year variation for patterns of neighbour shade in herbaceous communities.

We carried out two related experiments to test the transgenerational fitness effects of full sun versus simulated understorey shade as parental environments. The design allowed us to separately evaluate the effects of parental environment and genotype, and to test for genotypic differences in transgenerational effects. For a multi-population sample of five genotypes, we grew replicate parent plants in contrasting glasshouse light treatments and then examined the effects of parental sun versus shade on (a) progeny competitive performance and (b) total lifetime fitness in three alternative offspring environments: sunny dry conditions, severe understorey shade and neighbour shade. To gain insight to the causes of fitness variation, we also measured three growth traits: height extension, which plays a key role in competitive interactions [77] timing of reproductive onset, which can strongly affect lifetime reproductive output in plants [63,78], and total vegetative biomass, which contributes to reproductive potential [64]. These data provide evidence that transgenerational plasticity in response to parental shade may have a surprisingly strong positive effect on the ecological interactions and reproductive fitness of progeny growing in shade, but an even stronger negative effect on fitness if progeny instead encounter sunny, dry conditions.

2. Methods

(a) Study system

Polygonum persicaria is a common Eurasian annual plant naturalized in North America [79,80]. Previous studies have documented inherited effects of both parental moisture and parental light conditions on seedling development in this species [24,81,82]. In order to sample from the species' genotypic diversity, genotypes were drawn from three typical northeastern US populations: a moist pasture in full sun (MHF population Northfield, MA), a moist, moderately shaded field (TP population Dover, MA) and an organic farm (full sun with neighbour shade NAT population, Natick, MA see [65] for site details). Note that this multi-population sample is intended to provide a robust basis for (i) evaluating transgenerational effects in this species and (ii) testing for potential genotypic variation in these effects, and not to resolve the distribution of such variation within versus among populations see [24,26] for related studies using this same sample design. Field-collected achenes (one-seeded propagules) were inbred under uniform glasshouse conditions for four generations to produce highly inbred (selfed full-sib) genetic lines (hereafter ‘genotypes’).

(b) Parental generation

Replicate parent plants of each inbred genotype were grown in both sun and shade glasshouse treatments to produce genetically uniform offspring that differed only in parental light environment (see [26,81,83]).

Fifth-generation inbred achenes of 5 genotypes (2 MHF, 2 TP and 1 NAT see above) were stratified in distilled water at 4°C for seven weeks, sown into flats of moist vermiculite, and randomly positioned on a glasshouse bench (1 June 2012). At the first true leaf stage (4–6 days after emergence), seedlings of each genotype were individually transplanted into 1 l clay pots filled with a 1 : 1 : 1 mix of sterilized topsoil : horticultural sand : fritted clay (Turface™, Profile Products, Buffalo Grove, IL, USA) pre-moistened with 250 ml water. Five days after transplant, replicate seedlings of each genotype were randomly assigned to each of two parental glasshouse treatments. In the parental sun treatment, plants received 100% of incident light (ca 1300–1800 µmol m –2 s –1 midday photosynthetically active radiation (PAR)) with a red : far red (R : FR) spectral ratio of ca 1.0 (measured with an SKR R : FR meter Skye Instruments, Llandrindod Wells, UK). The parental shade treatment consisted of a metal frame covered by 80% neutral-density shade cloth (PAK Unlimited, GA, USA) overlaid with strips of green plastic filter (no. 138 Lee Filters, Burbank, CA, USA), providing plants with ca 260 µmol m –2 s –1 midday PAR and an R : FR ratio ≈ 0.7, which agrees with measured R : FR ratios in shaded natural Polygonum habitats [84]. Equidistant 3.5 cm diameter holes cut in the shade cloth provided parental shade plants with a daily 15 min sunfleck, simulating understorey conditions [85]. Parental plants in both treatments were kept at field capacity moisture and grown for nine weeks, with bench positions re-randomized weekly. Self-fertilized, full-sib achenes produced by the 10 experimental parent units (5 genotypes × 2 parental treatments) were harvested, air-dried and stored at 4°C.

(c) Competition experiment

For each genotype, 250 achenes from a parent plant grown in parental sun and 250 achenes of that genotype grown in parental shade were germinated in 100 mm Petri plates lined with moist filter paper and positioned randomly on a glasshouse bench (7 June 2017). Plates were monitored twice daily for germination. As soon as the radicle began to emerge, new germinants were immediately transplanted into 1 l clay pots (filled as described above but with a protective 1 cm top layer of moist vermiculite) in pentagonal competitive arrays that each consisted of a central target plant and five surrounding, equidistant neighbour (competitive background) plants. These spatial arrays were set up to test competitive interactions in all four possible combinations of parental sun or shade target plants, and parental sun or shade competitive backgrounds (i.e. parental sun target/parental sun background, parental sun target/parental shade background parental shade target/parental sun background parental shade target/parental shade background, figure 1a). For each genotype, 10 replicate arrays were set up for each of the four parental treatment combinations. The overall experimental design was: 5 genotypes × 2 parental treatments of target plant (target PT) × 2 parental treatments of competitive background plants (background PT) × 1 replicate array per block × 10 blocks = 200 competitive arrays.

Figure 1. Effects of parental light treatment on the performance of central target plants in competitive arrays. (a) Design and labelling of competitive arrays (one of four factorial arrays is shown as an example): one parental sun (S) target plant is surrounded by five parental shade (SH) background plants of the same genotype. Means ± s.e. for each type of array are shown (pooled across 5 P. persicaria genotypes) for (b) number of days to reproductive onset and (c) lifetime reproductive output. Letters indicate significant differences based on post hoc Tukey's HSD tests (details in Methods). (Online version in colour.)

Competitive arrays were set in a randomized complete block design (with separate blocks set across multiple glasshouse benches) under moderate shade tents (as described above in §2b) at ca 235 ± 32 µmol m –2 s –1 midday PAR (R : FR ≈ 0.7) and grown at 100% field capacity moisture for 13–14 weeks, a period of time corresponding to the full length of a natural growth season for the source Polygonum populations. The distance between individual plants in the competitive arrays (equivalent to 490 individuals per m 2 ) corresponds to high-density conditions observed in natural Polygonum field populations [86,87].

(d) Contrasting offspring treatments

Eight replicate offspring from each (genotype and parental treatment) experimental unit (1–3 replicate parent individuals per unit) were stratified (see §2a), germinated as described below, and grown in a randomized split-plot design in each of three glasshouse growth treatments: neighbour shade, severe shade and sunny dry. Plants were harvested after 13–14 weeks in treatment. In each treatment, midday light measurements were taken daily for 11 consecutive days (midway through the experiment) to calculate mean midday PAR, and six soil moisture measurements were taken (SM 150 soil moisture kit, Delta-T Devices, Cambridge, UK) to determine mean soil moisture. R : FR light wavelength ratios are reported based on prior studies using the same glasshouse treatments [84,88]. The experimental design was: 5 genotypes × 2 parental treatments × 3 offspring treatments × 8 blocked replicates per offspring treatment (total N = 240 plants).

Severe shade and sunny dry offspring treatments: for each genotype, 48 achenes produced by a parent individual grown in parental sun, and 48 achenes from a parent individual of the same genotype grown in parental shade, were sown as described in §2b (31 May 2017) and individually transplanted at the first true leaf stage into 1 l clay pots (see §2b 15 June 2017). In the severe shade treatment, plants were grown at 100% field capacity moisture under the shade tents described in §2b but with an additional layer of 30% neutral-density shade cloth (PAK Unlimited, GA, USA), resulting in midday PAR levels of ca 126 ± 20 µmol m −2 s −1 and R : FR ≈ 0.7. In the sunny dry treatment, plants received 100% of full glasshouse sun (ca 1569 ± 252 µmol m −2 s −1 midday PAR, R : FR ≈ 1) and were manually given 10–15 ml water 1–4 times per day as needed to maintain uniform moisture stress in all pots (ca 23% of soil field capacity by weight), such that every plant wilted for 2–3 h at midday.

Neighbour shade offspring treatment: the neighbour shade treatment was set up as described in §2c for competitive arrays, except that all plants in a single array were from the same genotype and parental treatment (8 pots per genotype×parental treatment combination).

(e) Data collection

Flowering (defined as the first day on which the open perianth of at least one flower on the plant was visible) was monitored daily to determine the number of days to reproductive onset. Plant height (cm from base to apex) was measured weekly in juvenile plants (weeks 3–6 in severe shade, sunny dry and neighbour shade treatments weeks 1–6 in the competition experiment). Starting at week 9 in treatment, mature achenes were collected weekly (to prevent the loss of ripe achenes), air-dried and weighed. At final harvest, vegetative and reproductive tissues (including mature and immature achenes, flowers and peduncles mature achenes typically compose ≥ 95% of reproductive tissue mass, S. E. Sultan 2001, unpublished data) were separately harvested. The air-dried masses of reproductive tissues collected at harvest were summed with previously collected achenes to determine lifetime reproductive output (g). Vegetative tissues were collected, dried at 100°C for ≥1 h and then at 65°C for ≥48 h, and weighed, to determine vegetative biomass (g). For the neighbour shade treatment and the competition experiment, traits were measured only for the target plant in each array. Owing to insufficient germination, nine drought-stressed plants that never reached maturity, and the exclusion of one to six outliers per trait (data points that >1.5 times the interquartile range below the first quartile or above the third quartile), the final samples sizes for each trait were N = 223 (days to reproductive onset), N = 225 (lifetime reproductive output), N = 238 (plant height) and N = 201 (vegetative biomass, owing to oven malfunction) in the contrasting offspring environments, and N = 189 (days to reproductive onset), N = 191 (lifetime reproductive output), N = 129 (vegetative biomass, owing to oven malfunction) and N = 193 (plant height) in the competition experiment.

(f) Data analysis

Statistical analyses were performed with JMP Pro 13 (SAS Institute, Cary, NC, USA) and graphing was done with R v. 3.3.3 (R Core Team 2017 Type I error was controlled using false discovery rate (FDR)-adjusted p-values following the Benjamini & Hochberg method, with an FDR of 5% [89].

(i) Competition experiment

Analysis of variance (ANOVA) with type III sums of squares was used to analyse the (fixed) effects on target plant traits of target parental treatment (PT), background PT, genotype, all two-way and three-way interactions and block. These main and interaction effects on plant height over time were tested by multivariate repeated-measures ANOVA [90] following a significant sphericity χ 2 test, multivariate Wilks' lambda was used to assess effect significance [91]. To examine the extent to which variation in lifetime reproductive output was explained by transgenerational effects on reproductive timing, we carried out analysis of covariance (ANCOVA), testing the main and interaction effects of target and background plant parental treatments, genotype and block, and including days to reproductive onset as a covariate. Genotype was treated as a fixed effect because the sample was drawn from specific populations representing the species' ecological breadth and used in previous studies [26]. Lifetime reproductive output and vegetative biomass were Box–Cox transformed to meet the ANOVA assumption of homoscedasticity. Effect sizes were calculated as partial eta-squared ( η p 2 ) [92], a metric that is robust for comparing effect sizes across traits within a single dataset [92,93].

To evaluate the magnitude of the main effects of target PT (averaged across both genotypes and background plant PT), we calculated the mean per cent change of all target plants due to their parents' light treatment, using the equation: 100% × (trait meanPARENTAL SHADE − trait meanPARENTAL SUN)/trait meanPARENTAL SUN. We similarly calculated the mean per cent change of target plants due to the parental treatment of the background plants. To precisely resolve significant target PT × background PT interaction effects, post hoc Tukey's honest significant difference (HSD) tests were carried out to test for differences between target plant trait means in the four types of competitive array. To examine possible genotype-specific effects of parental sun versus shade, we followed up significant genotype × target PT and genotype × background PT interaction terms with simple effects tests [94].

(ii) Contrasting offspring treatments

ANOVA with type III sums of squares was used to analyse the (fixed) effects on offspring traits of parental treatment (PT, parental shade versus parental sun), offspring treatment (OT, severe shade, neighbour shade or sunny dry), genotype, all two-way and three-way interactions and block (nested within offspring treatment) (see [26] for a similar analysis). We used ANCOVA to test these main and interaction effects on lifetime reproductive output while including day of reproductive onset as a covariate. As described above, multivariate repeated-measures ANOVA was used to analyse changes in plant height over time. Effect sizes were calculated as partial eta-squared ( η p 2 ) . All traits were Box–Cox transformed to meet the assumptions of ANOVA.

Significant (and marginally non-significant) parental treatment × offspring treatment interaction effects were followed with simple main effects tests of differences due to parental treatment within each offspring treatment. To further examine the offspring treatment-specific effects of parental treatment on each trait, the mean per cent change (pooled across genotypes) due to parental shade versus parental sun was calculated in each offspring treatment using the equation: 100% × (trait meanPARENTAL SHADE − trait meanPARENTAL SUN)/trait meanPARENTAL SUN. To examine genotype-specific effects, the significant genotype × parental treatment×offspring treatment three-way interaction effect was followed up with simple effects tests to separately assess for each genotype the effect of parental treatment within each offspring treatment.

3. Results

(a) Competition experiment

(i) Progeny of shaded parents showed enhanced performance for both competitive response to neighbours and competitive impact on them

Target plants that were progeny of shaded parents (averaged across the 5 genotypes and 2 background conditions) maintained high growth and fitness despite competition (competitive response), flowering 6.6 days earlier than parental sun target plants, growing 25% taller by week 6, and producing 47% greater vegetative biomass and 92% greater lifetime reproductive output (table 1, effect of target PT on all traits p < 0.0001*** figures 1 and 2). When competing against each type of competitive background (either sun progeny or shade progeny), parental shade target plants maintained higher fitness than parental sun targets (cf. Tukey's tests, figure 1b,c).

Figure 2. Effects of parental light treatment on target plant height extension over time in competitive arrays. Means ± s.e for each type of array are shown (pooled across 5 genotypes) parental treatment of target and background plants (parental sun, S parental shade, SH) labelled as in figure 1. Letters indicate significant differences based on post hoc Tukey's HSD tests (details in Methods). (Online version in colour.)

Table 1. Results of ANOVA for parental effects on competitive performance. Effects of parental treatment of target plant (target PT parental shade versus parental sun), parental treatment of competitive background (background PT parental shade versus parental sun) and genotype (G) on target plant fitness traits from three-way ANOVA. Significant p-values (adjusted for false discovery rate) and partial eta-squared ( η p 2 ) values for each term are shown in italics ( † p < 0.10, *p < 0.05, **p < 0.01, ***p < 0.001, non-significant p ≥ 0.10). Details in Methods.

a Owing to oven malfunction, block d.f. = 6 for target plant vegetative biomass.

The offspring of shaded parents were also better at competitively suppressing the growth and fitness of neighbours (competitive effect) than the offspring of full-sun parents. When grown with parental shade competitive backgrounds, target plants (averaged across both target parental treatments) flowered 2.3 days later than target plants competing with parental sun competitive backgrounds, grew 11% shorter, and produced 26% less vegetative biomass and 30% lower lifetime reproductive output (table 1: effect of background PT on all traits p < 0.0072**). Together, the positive effects of parental shade on both response as target plants and impact as background plants resulted in consistent rank ordering of target plant growth and fitness in the four combinatorial arrays: the tallest, earlier-reproducing, highest biomass and highest fitness target plants under competition were shade progeny competing against a competitive background of sun progeny, and the target plants with the lowest fitness were sun progeny competing against a competitive background of shade progeny (cf. Tukey's tests figures 1b,c and 2). Based on weekly height measurements, these effects did not diminish over developmental time, and indeed target progeny of sun parents increasingly reduced height extension (significant interaction effects of target PT×time, background PT×time table 2), especially when competing with a shade-progeny background (significant effect of target PT×background PT on height at week 6, table 1 Tukey's tests, figure 2). Based on ANCOVA, timing of reproductive onset was a significant covariate for lifetime reproductive output (p < 0.0001***), but the main effects of target PT and background PT on target plant fitness remained significant (p < 0.0235* and p < 0.0008***, respectively electronic supplementary material, table S1).

Table 2. Results of repeated-measures ANOVA for parental effects on height extension over time. Effects of parental treatment of target plant (target PT parental shade versus parental sun), parental treatment of competitive background (background PT parental shade versus parental sun), genotype (G) and time on target plant height measured weekly over six weeks from a multivariate repeated-measures ANOVA. Significant p-values (adjusted for false discovery rate) are shown in italics († p < 0.10, *p < 0.05, **p < 0.01, ***p < 0.001, non-significant (n.s.) p ≥ 0.10). Details in Methods.

(ii) Effects of parental shade versus sun on competitive performance varied among genotypes

Polygonum genotypes varied in the impact of parental shade versus sun on target plant performance (significant genotype×target PT interaction effects for all traits table 1). Genotype by parent treatment interaction effects on the competitive impact of background plants was also highly significant for lifetime reproductive output, but marginally non-significant for growth traits (genotype × background PT effects table 1 see electronic supplementary material, figure S1 for effects of target PT and background PT on individual genotypes). Genotypic differences for the effects of both target and competitive background parent treatment significantly affected height over time (significant effects of genotype × target PT × time and genotype × background PT × time table 2).

For every target-plant trait (except number of days to reproductive onset), the target PT and background PT together explained more variation than genotype (cf. η p 2 values, table 1: target PT η 2 ≈ 0.18–0.28 background PT ≈ 0.09–0.12 and genotype ≈ 0.22–0.29 for those three traits). For lifetime reproductive output, the combined effects of target PT and background PT explained more variation than did genotype, and the parental environment of the target plant alone had virtually equivalent impact on fitness to its genotype (table 1: η p 2 = 0.284 , 0.116 and 0.289, respectively). However, genotype explained substantially more of the variation for number of days to reproductive onset (table 1: η p 2 : target PT = 0.351 background PT = 0.052 and genotype = 0.591).

(b) Contrasting offspring treatments

(i) Parental shade increased growth and fitness of progeny in both severe and neighbour shade, but reduced growth and fitness in sunny, dry conditions

Parental treatment resulted in substantial, lifetime effects on progeny growth and fitness these effects varied significantly depending on offspring treatment (table 3, PT × OT interaction effects on all traits p < 0.0001*** figure 3). Because the effects of parental shade versus sun were positive in the two progeny shade treatments but negative in the progeny sun treatment, the main effect of parental treatment was generally non-significant (table 3). In both severe and neighbour shade, progeny of shaded parents grew taller and larger, and had earlier reproductive onset and greater lifetime reproductive output, than progeny of full-sun parents. However, shade-produced progeny were shorter, smaller in biomass, slower to reproduce and less fecund than progeny of full-sun parents in the sunny dry offspring treatment (figure 3a–d).

Figure 3. Effects of parental sun versus parental shade on fitness traits of offspring grown in contrasting treatments. Means ± s.e are shown (pooled across 5 genotypes) for (a) plant height at week 6, (b) total vegetative biomass, (c) number of days to reproductive onset and (d) lifetime reproductive output. For each trait, significance tests for the effect of parental shade versus parental sun within each offspring treatment are shown (simple effects tests † p < 0.10, *p < 0.05, **p < 0.01, ***p < 0.001, non-significant (n.s.) p ≥ 0.10 details in Methods). Insets show enlarged scale for significant or marginally n.s. results within stressful, low-growth treatments. (Online version in colour.)

Table 3. Results of ANOVA for parental effects on growth and fitness in contrasting environments. Effects of parental treatment (PT parental shade versus parental sun), offspring treatment (OT severe shade versus neighbour shade versus sunny dry), genotype (G), all two- and three-way interactions and block (nested within offspring treatment) on growth and fitness traits, based on significance tests from a three-way ANOVA. Significant p-values (adjusted for false discovery rate) and partial eta-squared (η 2 p) values for each term are shown in italics ( † p < 0.10, *p < 0.05, **p < 0.01, ***p < 0.001, non-significant p ≥ 0.10). Details in Methods.

a Owing to oven malfunction, block d.f. = 18 for vegetative biomass.

In the severe shade and neighbour shade treatments, juvenile progeny of shaded parents grew significantly taller than progeny of full-sun parents (by 19 and 13%, respectively p = 0.028* and 0.003** based on simple effects test of parental treatment within each offspring treatment figure 3a). This height increment was consistent over time (electronic supplementary material, figure S2a,b parental treatment×time interaction effects 0.269 > p > 0.074). In the sunny dry treatment, by contrast, progeny of shaded parents initially expressed this same height advantage, but starting in week 4 they became shorter than sun-parent progeny, a height gap that became more pronounced over time as the shade progeny increasingly slowed shoot extension (electronic supplementary material, figure S2c parental treatment × time interaction p = 0.039*). By harvest, the offspring of shaded parents had produced significantly more vegetative biomass than the offspring of full-sun parents in severe offspring shade (+57% p < 0.0188), and slightly (non-significantly) more in neighbour shade (+8% p = 0.702 figure 3b). However, for offspring grown in sunny dry conditions, parental shade resulted in dramatically decreased vegetative biomass compared with parental sun (−61%, p < 0.0001*** figure 3b).

Offspring of shaded parents transitioned to reproduction earlier than offspring of full-sun parents in both severe shade and neighbour shade (8 and 22% earlier, respectively p ≤ 0.023* figure 3c). Parental-environment effects on fitness were surprisingly dramatic: parental shade resulted in 55% greater lifetime reproductive output compared with parental sun for progeny in severe shade (p ≤ 0.0228*), and 53% higher reproductive output in neighbour shade (p = 0.0117*) (figure 3d). Conversely, in sunny dry conditions, the offspring of shaded parents had a 20% later reproductive onset (p < 0.0001*** figure 3c) and 71% lower lifetime reproductive output (p < 0.0001*** figure 3d) than offspring of full-sun parents. The impact of parental treatment on lifetime fitness in contrasting environments was not entirely explained by effects on reproductive timing: although reproductive onset was a significant covariate for total reproductive output (p < 0.0001***), both the main effect of parental treatment and the PT × OT interaction remained significant after acccounting for this effect (p < 0.0355* and p < 0.0002***, respectively, in ANCOVA electronic supplementary material, table S1).

(ii) Effects of parental and offspring treatment varied among genotypes

For most traits, the effects of parental as well as progeny treatment varied among genotypes (significant genotype × PT effects on reproductive onset and total fitness significant genotype × OT effects on these traits as well as on plant height and three-way genotype × PT × OT effects on reproductive onset and (marginally non-significantly) plant height table 3). Such three-way interactions reflect the particular impact of parental environment on each genotype's pattern of trait expression in the three alternative progeny growth environments (figure 4). For instance, parental shade led to substantially faster reproductive onset for plants of genotype NAT 2 growing in neighbour shade, and a less pronounced but similar effect in severe shade, while plants of genotype MHF 1 showed a pronounced (negative) effect of parental shade on reproductive onset in the sunny dry progeny treatment, but no effect on life-history timing in the shade treatments (figure 4)

Figure 4. Effects of parental sun versus parental shade on each genotype's time of reproductive onset in three contrasting offspring treatments. Means ± s.e. are shown. For each genotype, significance tests for the effect of parental shade versus parental sun within each offspring treatment are shown (simple effects tests † p < 0.10, *p < 0.05, ***p < 0.001, non-significant (n.s.) p ≥ 0.10 details in Methods). (Online version in colour.)

The main effect of genotype was significant or marginally non-significant for all traits (table 3). However, with one exception (reproductive onset timing), differences due to offspring treatment-specific effects of parental treatment were greater than those due to genotype (η 2 p values, table 3 e.g. for total reproductive output, η p 2 = 0.277 for PT × OT interaction effect and η p 2 = 0.130 for genotype). Note that, because experimental genotypes were drawn from three distinct populations and thus were not closely related, our sample likely includes large genotypic differences (e.g. relative to genotypic differences within a single natural population). Accordingly, this was a conservative way to test the relative magnitude of inherited environmental versus genotype effects.

4. Discussion

(a) Parental shade significantly enhanced the competitive ability of offspring in shade

Because plants do not grow in isolation, competitive ability is a key fitness factor in natural populations [95,96]. This ability arises from two distinct aspects of plant performance: competitive effect, the ability to suppress the growth and reproduction of neighbour individuals, and competitive response, the ability to maintain growth and fitness despite the presence of neighbours [97,98]. Success relative to neighbours may result from either aspect of competitive ability [96] the two are often positively correlated (e.g. [99–103]), but in some systems, individuals show just one type of competitive superiority [97,98,104,105]. We tested the effect of parental shade versus sun on each aspect of competitive ability by factorially varying the parental treatment of competing focal (target) and background plants. Both competitive response and competitive effect were substantially greater in progeny of shaded parents than progeny of full-sun parents: as target plants, they more successfully maintained high growth rates, early reproductive onset, and total reproductive output against a background of competing individuals, and as background plants, they more effectively suppressed the growth and fitness of target plants.

Such among-individual variation in competitive ability is generally assumed to result from genetic differences, and indeed many studies have confirmed that genotypes may differ in one or both aspects of competitive ability (e.g. [104,106–113]), including in a closely related Polygonum species [114]. By contrast, the possible influence of parental environment on competitive interactions has seldom been rigorously tested (i.e. by holding genotype constant [49]). Here, we present the first evidence for a substantial and specifically adaptive effect of parental environment on competitive ability in a similar (shade) environment. Notably, although the growth and fitness of target plants in competitive arrays differed on average among Polygonum genotypes, more of the variation in height, biomass and lifetime reproductive output was explained by the parental treatments of the target and background plants than by their genotype, and the parental environment of just the target plant had as great an impact on its reproductive output as did its genotype. This finding raises the possibility that competitive outcomes in plant populations may be strongly shaped by environmentally induced transgenerational effects as well as by genotype.

Earlier studies have shown ‘silver-spoon’ environmental effects, in which progeny of resource-poor or environmentally stressed maternal individuals have lower growth and reproduction in competition than progeny of resource-rich mothers (e.g. [41,43] reviewed in [40,115]). In other cases, resource-deprived maternal animals and plants (such as those grown at higher density) may express adaptive offspring size plasticity [116] by producing larger or higher-quality eggs or seeds [49,56,117] that are able to grow successfully under competitive conditions. Whether negative or positive, such overall provisioning effects are likely to influence growth and hence competitive performance in any offspring environment.

By contrast, the superior competitive effect and response of shade-produced Polygonum progeny likely reflect the specific developmental effects of parental shade on progeny height and shading power, two traits that allow plants to overtop and thereby suppress competitors while maximizing their own access to available photons ([77] e.g. [118–122]). Along with the greater rate of height extension documented here—an effect that increased over time in contrast to expectations (see below, §4b last paragraph)—a previous study with the same P. persicaria genotypes and glasshouse treatments showed that seedling progeny of shaded parents produced more vegetative biomass, increased allocation to leaf tissue and produced larger, thinner leaves, resulting in greater whole-plant leaf area [82].

Unlike the ‘silver-spoon’ effects on competition discussed above, shaded P. persicaria parents altered these specific developmental traits of offspring without increasing overall provisioning [82]. Moreover, expression of these inherited environmental effects was context-dependent: trait changes due to parental shade were more pronounced when progeny were grown in glasshouse shade that mimicked the spectral signal of neighbour or canopy vegetation than in full sun [82]. Such specific changes to phenotypic expression of offspring may result from environmentally induced parental adjustments to cytoplasmic signalling constituents of egg or seed tissues, such as hormones, small or noncoding RNAs, and proteins, or to environment-specific epigenetic modifications of DNA [34,123–125]. Previous work with P. persicaria has confirmed that DNA methylation changes substantially mediate the transgenerational developmental effects of both shade and drought stress in this system [82,83]. Note that here we present data documenting the effects of parental shade on progeny competitive ability only in a shaded progeny treatment. Because the expression of specific transgenerational modifications (as well as possible fitness costs of those trait states) may vary depending on offspring conditions, the competitive consequences of parental shade effects could well differ in direction and/ or magnitude in alternative abiotic progeny conditions such as dry soil or intense insolation.

(b) Parental shade increased progeny growth and fitness in both severe and neighbour shade, but reduced growth and fitness in sunny, dry conditions

Contrasting parental light environments caused surprisingly large (and highly significant) fitness differences over the full life cycle of P. persicaria progeny. Offspring of shaded parents had faster reproductive onset and considerably higher lifetime reproductive output when grown in both severe simulated understorey shade and neighbour shade. These data provide one of very few documented examples of specifically adaptive transgenerational effects of parental conditions on the lifetime reproductive fitness of progeny in similar environments. To our knowledge, such fitness effects have previously been shown only in food-limited mosquitoes [53] and in planktonic marine crustaceans exposed to pathogens [52] or heavy metals [54]. Our data also revealed a substantial negative fitness effect of parental shade on progeny grown in dissimilar conditions: in a sunny, dry environment, the offspring of shaded parents had delayed reproductive onset and dramatically decreased lifetime reproductive output relative to progeny of parents that had grown in full sun. These findings indicate that, at least in certain taxa, environmental conditions experienced by parent individuals may lead to strongly adaptive or maladaptive effects on fitness, depending on progeny conditions. Note that the pronounced fitness effects of parental environment were not driven solely by changes in phenology, as these effects were highly significant even after accounting for flowering time as a covariate.

Most of the (relatively few) cases in which parental conditions have been shown to influence lifetime fitness of progeny reflect direct provisioning changes that consistently either reduce or enhance progeny growth (e.g. [45] discussed in §4a above). By contrast, P. persicaria progeny showed context-dependent fitness effects that likely reflect specific transgenerational adjustments: as noted above, in a previous study with these same genotypes, progeny of shaded parents produced shade-appropriate phenotypes with greater leaf allocation and larger, thinner leaves [82]. Functionally, the resulting increase in photosynthetic surface area per unit plant mass would maximize growth in either canopy or neighbour shade [68,69,126–129]—as indicated by the higher total biomass of shade progeny in these conditions—but could also account for the maladaptive growth and fitness effects of parental shade on offspring in sunny, dry conditions, where larger, structurally thinner leaves would lose more water to transpiration [69]. In a different set of P. persicaria genotypes, offspring of low-light parents had equal biomass but significantly shorter roots by day 3 of development than offspring of isogenic full-sun parents [81], a developmental adjustment that would likewise be maladaptive in dry soil, where seedlings must quickly extend roots to gain access to available moisture [130–132].

The significantly greater lifetime fitness of shade-produced P. persicaria offspring that were themselves grown in shade treatments exemplifies adaptive transgenerational plasticity, in which parent individuals respond to environmental conditions by altering their progeny in ways that are specifically adaptive to those conditions (see [17–33]). Clearly, the fitness impact of these plastic adjustments will depend on whether progeny encounter similar or contrasting environmental challenges the transgenerational effect of parental shade on fitness of progeny in sunny, dry conditions was even more strongly negative. When parent and offspring environments match, such specific transgenerational effects may help populations to persist in altered or stressful conditions, by allowing many individuals in the progeny generation to maintain fitness without the lag time (and serendipity) required for favourable allelic variants to selectively increase [34,37,47,133]. Yet when progeny encounter a different environmental state than that of the parent—for example, in the case of passive dispersal across a patchy landscape, or a temporal change in situ from one generation to the next—transgenerational developmental modifications can result in reduced fitness that may likewise be expressed in many individuals at once [50,60,134–136].

Although parental light environment clearly has a pronounced impact in P. persicaria, the extent to which such inherited effects may be important for realized fitness outcomes more generally, and in natural populations, is not yet known. Evidence for parental effects on lifetime competitive success and reproductive fitness may be lacking because studies have seldom tested for them: because any effects of parental environments on offspring phenotypes are generally expected to diminish during ontogeny ([50,137] e.g. [29,33,138,139]), many studies that have identified putatively adaptive transgenerational effects have measured only developmental traits expressed early in the life cycle ([21], but see [23,26] for data on juvenile mortality). Similarly, studies of epigenetically mediated inherited effects (e.g. methylation changes in plants) have rarely examined fitness consequences directly [25,140,141], but have focused instead on differences in developmental and reproductive timing, allocation, and herbivore damage [140,142,143], or on gene expression changes [144]. In a careful meta-analysis of 58 transgenerational studies, Uller et al. [50] found that effects of parental environment on putatively fitness-related functional and developmental traits were generally ‘subtle’ compared with direct effects of the offspring's immediate environment. However, their analysis showed that the impact of parental environment on offspring traits varied enormously among studies, as well as among traits within studies (see also [38,137]). Like other aspects of plasticity, transgenerational effects will no doubt vary for different taxa, environmental states and progeny traits. A broader understanding of the possible impact of such effects in natural populations will require lifetime fitness data from appropriately designed experiments with diverse biological systems, in naturalistic alternative environments [50].

(c) Transgenerational effects of parental shade versus sun on competitive performance and fitness varied among genotypes

In addition to generally small but significant (or marginally non-significant) average differences, the five P. persicaria genotypes varied significantly in the effects of parental light environment on competitive and fitness traits of their progeny. Just as genotypes vary in their plastic responses to the immediate environment (references in [133,145,146]), genotypic variation for transgenerational plasticity is a common if not ubiquitous feature of these systems [61] that has been documented previously in other genotypes of P. persicaria [81,83] as well as many other plant and animal taxa (e.g. [49,147–151]). Such statistical genotype by parental environment effects reflect the influence of inherited, environmentally induced modulations of cytoplasmic and epigenetic signalling factors on the progeny individual's gene expression pathways (references in [133]). Hence, although heritable parent environment effects are often considered to be ‘decoupled’ from genetic variation [37], the two modes of inheritance interact, resulting in genotype-specific patterns of transgenerational plasticity ([83,151–154]). When such variation occurs within populations, it may provide a substrate for further adaptive evolution of parental effects [20,147,148,155]. Although our multi-population sample of genotypes was not designed to address this issue, the pronounced differences between the two pairs of genotypes drawn from the same populations (MHF 1 and 2, and NAT 1 and 2 figure 4) suggest that this type of variation is likely present in this system, but there is no indication in this limited sample of consistent population differences.

Because our design allowed us to test the effects of both parent and offspring treatment on individual genotypes, the results revealed an even more complex aspect of biological interaction. As discussed (see §4b), the fitness impact of parental shade versus sun was very different in alternative progeny environments, demonstrating how inherited and immediate environmental factors jointly shape individual phenotypic outcomes [24,34,82,137]. Genotypes also differed in their responses to both parental and immediate conditions, leading to genotype by environment by parent environment interactions that were statistically significant for reproductive onset (and nearly so for plant height, a key competitive trait). Plasticity studies use the term norm of reaction to describe an individual's pattern of phenotypic response to a given set of environments, such as the contrasting offspring treatments we studied ([145,156] reviewed in [133]). This characteristic response pattern is usually considered to be genetically determined [35,157,158]. These results suggest that, instead, the norm of reaction entails response to a particular combination of parental and immediate environments [38,152]. For example, the effect of parental shade versus sun on reproductive onset in the P. persicaria genotypes was not to move their response norms similarly up or down, as would be predicted by a ‘silver spoon’ parental effect on overall offspring size or quality. Instead, the impact of parental environment on norms of reaction varied, depending on the particular genotype in question (cf. figure 4).

These data thus illustrate at the genotype level a view of transgenerational plasticity as ‘differences in offspring phenotype that occur due to the interaction between the current generation and the previous generation's environmental conditions' ([21], cited in [38]). Such highly complex effects on fitness-related traits can be expected to render natural selection based on genetic variants per se less efficient, altering selective trajectories on those variants, and potentially maintaining allelic variation in environmentally heterogeneous populations ([34,159–162] further references in [133]). Conversely, if patterns of environmental variation are predictable within or across generations, and complex genotypic fitness differences are therefore consistently expressed, selection may shape the particular way a population integrates parental with immediate environmental factors to most effectively generate adaptive phenotypes [38,50,163–165]. This would lead to population-specific patterns of genotype by environment by parent environment interactions, rather than to simpler among-population differences in transgenerational effects per se. Testing for such potentially complex aspects of local adaptation poses a fascinating question but is beyond the scope of the present study: this requires comparing populations from sites that differ in quantified patterns of both environmental variation and temporal autocorrelation.

5. Conclusion

Both empiricists and theoreticians have emphasized the importance of a better understanding of plasticity—including transgenerational plasticity—to assess the prospects for adaptation to rapidly changing environments [35,38,50,166]. This consensus reflects the realization that it is not DNA sequence variation alone that will determine the potential for future adaptation, but rather the phenotypes that are actually expressed in future environments and their fitness consequences [2,38,167,168]. We identified strong adaptive and maladaptive effects of parental shade on both the competitive performance and the lifetime reproductive output of progeny, depending on whether the progeny were themselves growing in shaded or sunny, dry conditions. These data make clear that parental environment may substantially influence not only the early development but also the fitness of offspring, in ways that depend in turn on offspring environment. When adaptive transgenerational effects are context-dependent, as in this case, their potential contribution to adaptive rescue will depend on the precise distribution of environmental states, both spatially (with respect to dispersal) and temporally. Furthermore, when genotypes vary in these context-dependent effects, further adaptive evolution of transgenerational effects may be subject to complex selective dynamics, especially if environmental conditions become more variable in the future. Further studies testing genotypic responses to realistic combinations of parental and progeny environments may provide critical insights to the potential for future adaptation in diverse natural systems.

Data accessibility

The datasets generated and analysed for this study are available as part of the electronic supplementary material.