Requirements for the evolution of evolvability

We have aready discussed how selection can bias variation to be more advantageous, but what are the the requirements for this to happen?
This paper from our colleagues at Southampton models gene regulatory network evolution to address which factors allow the generation of phenotypic variation "tailored" to environmental variation.

10:00 in Darwin's, with fika.

Paper available here

Abstract

One of the most intriguing questions in evolution is how organisms exhibit suitable pheno- typic variation to rapidly adapt in novel selective environments. Such variability is crucial for evolvability, but poorly understood. In particular, how can natural selection favour develop- mental organisations that facilitate adaptive evolution in previously unseen environments? Such a capacity suggests foresight that is incompatible with the short-sighted concept of natural selection. A potential resolution is provided by the idea that evolution may discover and exploit information not only about the particular phenotypes selected in the past, but their underlying structural regularities: new phenotypes, with the same underlying regulari- ties, but novel particulars, may then be useful in new environments. If true, we still need to understand the conditions in which natural selection will discover such deep regularities rather than exploiting ‘quick fixes’ (i.e., fixes that provide adaptive phenotypes in the short term, but limit future evolvability). Here we argue that the ability of evolution to discover such regularities is formally analogous to learning principles, familiar in humans and machines, that enable generalisation from past experience. Conversely, natural selection that fails to enhance evolvability is directly analogous to the learning problem of over-fitting and the sub- sequent failure to generalise.Wesupport the conclusion that evolving systems and learning systems are different instantiations of the same algorithmic principles by showing that exist- ing results from the learning domain can be transferred to the evolution domain. Specifically, we show that conditions that alleviate over-fitting in learning systems successfully predict which biological conditions (e.g., environmental variation, regularity, noise or a pressure for developmental simplicity) enhance evolvability. This equivalence provides access to a well- developed theoretical framework from learning theory that enables a characterisation of the general conditions for the evolution of evolvability.

On the non-random effects of random mutation

The idea that evolution produces (developmental) genetic architectures that make the effects of mutations biased towards particular phenotypes have come up a few times in recent discussions. Next week we will look a little closer at one of the models that have been used to explore the how and why of this problem.

10.00 in Darwin. Fika and entertainment provided.

 You can find the paper here

Epistasis and natural selection shape the mutational architecture of complex traits

Adam G Jones, Reinhard Burger & Stevan Arnold

The evolutionary trajectories of complex traits are constrained by levels of genetic variation as well as genetic correlations among traits. As the ultimate source of all genetic variation is mutation, the distribution of mutations entering populations profoundly affects standing variation and genetic correlations. Here we use an individual-based simulation model to investigate how natural selection and gene interactions (that is, epistasis) shape the evolution of mutational processes affecting complex traits. We find that the presence of epistasis allows natural selection to mould the distribution of mutations, such that mutational effects align with the selection surface. Consequently, novel mutations tend to be more compatible with the current forces of selection acting on the population. These results suggest that in many cases mutational effects should be seen as an outcome of natural selection rather than as an unbiased source of genetic variation that is independent of other evolutionary processes.

Sex difference in lifespan and sexual conflict

For the next week's lab meeting, I would like to use this Drosophila paper as a case, to discuss  the evolution of sexual dimorphism in lifespan. 

Hope to hear your thoughts over fika!

Photo by Qinyang Li

Manipulation of feeding regime alters sexual dimorphism for lifespan and reduces sexual conflict in Drosophila melanogaster

24.04.2017, 15:58 byElizabeth M. L. DuxburyWayne G. RostantTracey Chapman

Sexual dimorphism for lifespan (SDL) is widespread, but poorly understood. A leading hypothesis, which we test here, is that strong SDL can reduce sexual conflict, by allowing each sex to maximize its sex-specific fitness. We used replicated experimental evolution lines of the fruit fly, Drosophila melanogaster, which had been maintained for over 360 generations on either unpredictable ‘Random’ or predictable ‘Regular’ feeding regimes. This evolutionary manipulation of feeding regime led to robust, enhanced SDL in Random over control, Regular lines. Enhanced SDL was associated with a significant increase in the fitness of focal males, tested with wild-type (WT) females. This was due to sex-specific changes to male life history, manifested as increased early reproductive output and reduced survival. In contrast, focal female fitness, tested with WT males, did not differ across regimes. Hence increased SDL was associated with a reduction in sexual conflict, which increased male fitness and maintained fitness in females. Differences in SDL were not associated with developmental time or developmental survival. Overall, the results showed that the expression of enhanced SDL, resulting from experimental evolution of feeding regimes, was associated with male-specific changes in life history, leading to increased fitness and reduced sexual conflict.

One gene to rule them all (in a phylogeny)?

To what extent can one gene (or a handful of them) affect a phylogeny? This paper suggest that even in very large data matrices the resolution of some branches can rely on tiny subsets of data. They show this to be the case in several contentious nodes of plant, animal and fungi data matrices and suggest a framework for quantifying the phylogenetic signal in such difficult cases. 

They also think that humans are more closely related to sponges than ctenophores, which is cool. 

Darwin, 9th of May, 10.00. Blueberry pie to compensate the phylogeny topic.

Contentious relationships in phylogenomic studies can be driven by a handful of genes

Xing-Xing Shen, Chris Todd Hittinger & Antonis Rokas

Phylogenomic studies have resolved countless branches of the tree of life, but remain strongly contradictory on certain, contentious relationships. Here, we use a maximum likelihood framework to quantify the distribution of phylogenetic signal among genes and sites for 17 contentious branches and 6 well-established control branches in plant, animal and fungal phylogenomic data matrices. We find that resolution in some of these 17 branches rests on a single gene or a few sites, and that removal of a single gene in concatenation analyses or a single site from every gene in coalescence-based analyses diminishes support and can alter the inferred topology. These results suggest that tiny subsets of very large data matrices drive the resolution of specific internodes, providing a dissection of the distribution of support and observed incongruence in phylogenomic analyses. We submit that quantifying the distribution of phylogenetic signal in phylogenomic data is essential for evaluating whether branches, especially contentious ones, are truly resolved. Finally, we offer one detailed example of such an evaluation for the controversy regarding the earliest-branching metazoan phylum, for which examination of the distributions of gene-wise and site-wise phylogenetic signal across eight data matrices consistently supports ctenophores as the sister group to all other metazoans.

A plastic Daphnia stuck in the G matrix...

Heja!

Paper for next Tuesday:

The alignment between phenotypic plasticity, the major axis of genetic variation and the response to selection
Martin I. Lind, Kylie Yarlett, Julia Reger, Mauricio J. Carter and Andrew P. Beckerman
Proc. R. Soc. B 282: 20151651.
Link to paper




Abstract:
Phenotypic plasticity is the ability of a genotype to produce more than one phenotype in order to match the environment. Recent theory proposes that the major axis of genetic variation in a phenotypically plastic population can align with the direction of selection. Therefore, theory predicts that plasticity directly aids adaptation by increasing genetic variation in the direction favoured by selection and reflected in plasticity. We evaluated this theory in the freshwater crustaceanDaphnia pulex, facingpredation risk fromtwo contrasting size-selective predators. We estimated plasticity in several life-history traits, the G matrix of these traits, the selection gradients on reproduction and survival, and the predicted responses to selection. Using these data, we tested whether the genetic lines of least resistance and the predicted response to selection alignedwith plasticity. We found predator environment-specific G matrices, but shared genetic architecture across environments resulted in more constraint in the G matrix than in the plasticity of the traits, sometimes preventing alignment of the two. However, as the importance of survival selection increased, the difference between environments in their predicted response to selection increased and resulted in closer alignment between the plasticity and the predicted selection response. Therefore, plasticity may indeed aid adaptation to new environments.

Where?   Darwin
When?    May 2, 10.00 am

There will be fika, of course.

Epistasis and pleiotropy affecting modularity

Recently we have discussed modularity a few times. For those who can't get enough of it: here is another paper. For those who are starting to get fed up with it: focus on the cool results and the methods we animal ecologist can only dream of.

Fika will be provided.
Tuesday, April 25, 10.00 in Darwin.

Epistasis and Pleiotropy Affect the Modularity of the Genotype–Phenotype Map of Cross-Resistance in HIV-1

Robert Polster  Christos J. Petropoulos  Sebastian Bonhoeffer  Frédéric Guillaume
Mol Biol Evol (2016) 33 (12): 3213-3225

DOI: https://doi.org/10.1093/molbev/msw206

Abstract

The genotype–phenotype (GP) map is a central concept in evolutionary biology as it describes the mapping of molecular genetic variation onto phenotypic trait variation. Our understanding of that mapping remains partial, especially when trying to link functional clustering of pleiotropic gene effects with patterns of phenotypic trait co-variation. Only on rare occasions have studies been able to fully explore that link and tend to show poor correspondence between modular structures within the GP map and among phenotypes. By dissecting the structure of the GP map of the replicative capacity of HIV-1 in 15 drug environments, we provide a detailed view of that mapping from mutational pleiotropic variation to phenotypic co-variation, including epistatic effects of a set of amino-acid substitutions in the reverse transcriptase and protease genes. We show that epistasis increases the pleiotropic degree of single mutations and provides modularity to the GP map of drug resistance in HIV-1. Moreover, modules of epistatic pleiotropic effects within the GP map match the phenotypic modules of correlated replicative capacity among drug classes. Epistasis thus increases the evolvability of cross-resistance in HIV by providing more drug- and class-specific pleiotropic profiles to the main effects of the mutations. We discuss the implications for the evolution of cross-resistance in HIV.

Guest seminar by Thomas Madsen

Some of you might have heard about Sweden's southernmost adder population in Smygehuk and the spectacular rescue action in the 90s that even made it into Nature. The man behind the story, Thomas Madsen from Deakin University, AU, is currently visiting Sweden to continue his work on this snake population (they are still going strong!).
Before he disappears back to Australia again, he'll give a seminar at our EXEB meeting on Tuesday, April 18th. While his research interest has recently branched out to cancer in the Tasmanian devil (see e.g. here and here), he'll tell us about predator-prey dynamics between snakes and rats!

Floods and famine: climate-induced collapse of a tropical predator-prey community

Beata Ujvari and Thomas Madsen

Summary

1.     Will climate change threaten wildlife populations by gradual shifts in mean conditions, or by increased frequency of extreme weather events? 

2.     Based on long-term data (from 1991 to 2014), the aim of the present study was to analyze and compare the sensitivity of predator-prey demography to extreme climatic events versus normal, albeit highly variable, annual deviations in climatic conditions in the Australian wet-dry tropics. 

3.     From 1991 to 2005, predators (water pythons, Liasis fuscus) and their main prey (dusky rats, Rattus colletti) showed significant climate-driven fluctuations in numbers. 

4.     These fluctuations were, however, trivial compared to the impact of two massive but brief deluges in 2007 and 2011, which virtually eliminated the dusky rats.  The two floods resulted in the pythons experiencing an unprecedented famine in 7 out of the last 8 years causing a massive shift in python demography i.e. a significant reduction in feeding rates, reproductive output, growth rates, relative body mass, survival, mean body length and numbers (from 3173 in 1992 to 96 in 2013). 

5.     Our results demonstrate that attempts to predict faunal responses to climate change, even if based on long-term studies, may be doomed to failure.  Consequently, biologists may need to confront the uncomfortable truth that increased frequency of brief unpredictable bouts of extreme weather can influence populations far more than gradual deviations in mean climatic conditions.

There will be fika!

Time: Tuesday, April 18, 10.00

Locale: "Darwin", 2nd floor (Ecology Building)

Marvin's master's thesis

Macrostomum lignano. Picture courtesy of Lukas Schärer.

Marvin Moosmann will present his master's thesis next week on Tuesday April 11th at 10.00 in Darwin. The opponent will be Charlie Cornwallis.

Thesis abstract: The relationship between the male and the female function in the simultaneous hermaphroditic flatworm Macrostomum lignano has been intensively studied on a phenotypic level. The results from these studies largely coincide with predictions that derive from sex allocation theory, which assumes a trade-off between the allocation of resources to the sex functions. Results from a recent experimental evolution study suggest that sexually antagonistic genetic variation could also have an impact on the correlation between male and female fitness. Sexually antagonistic genetic variation manifests itself in a negative genetic correlation between male and female fitness and has so far mainly been described in separate-sexed organisms. This study investigates the phenotypic and genetic correlation between the male and female fitness components in M. lignano in two stressful environments; salt stress and food stress. The results suggest that there is no genetic or phenotypic correlation between male and female fitness, despite considerable genetic variation in fitness for both sex functions. However, the residual variation shows a tendency for a negative correlation in a food-restricted environment, which could be an indication of a resource trade-off that is obscured on a phenotypic level by the genetic variation in fitness. It was further found that the genetic variances of both fitness functions are environment dependent.

Research presentation by Hanna Bensch on "the monoculture effect" on April 4

For next week's EXEB-meeting, I am pleased to welcome one of our most beloved and loyal co-workers: Hanna Bensch. Hanna has been working for many summers now with us in the damselfly project, and she also participated in our recent field sampling expedition to Cameroon in Central Africa, during January and February 2017. Hanna's skills as a field assistant are amazing, and we are so happy that she has been working with us for so long time.

Hanna will give a presentation of her Master's-thesis work that she has done under the supervision of Charlie Cornwallis on ostriches (Struthio camelus) in South  Africa. The title is:

The monoculture effect: a meta-analysis and experiment on ostrich chicks

Abstract:

Increased genetic diversity of a population can decrease pathogen and parasite transmission and prevalence within the population, a phenomenon known as the monoculture effect. This diversity-disease hypothesis has been studied within many different host systems. However, the overall generality of the monoculture effect has been debated and not systematically investigated. I therefore tested the strength and generality of the monoculture effect by conducting a meta-analysis on the relationship between within group genetic diversity and pathogen prevalence or mortality. My meta-analysis confirmed the monoculture effect to be a general phenomenon, finding a significant negative relationship between group genetic diversity and rates of host infection and mortality. However, a majority of the studies included were on insects and further studies on a broader range of taxa is of interest to increase the understanding of the monoculture effect. To complement my meta-analysis, I therefore conducted an experimental study on ostrich chicks, testing group genetic diversity’s effect on growth and survival. 

 

 

If you want to know if chicks from groups of high diversity did better than chicks from groups of low diversity, then you have to come to my presentation! :)

 

 

Along the same topic as Hanna's presentation above, I suggest that we also have a discussion about a recent paper in Science about the relationship between resistance and tolerance evolution, that challenges the common view that these two forms of defense are redundant to each other. You can find the paper here, and the Abstract is below:

Antibiotic tolerance facilitates the evolution of resistance

1. Irit Levin-Reisman¹,
2. Irine Ronin¹,
3. Orit Gefen¹,
4. Ilan Braniss¹,
5. Noam Shoresh²,
6. Nathalie Q. Balaban¹,*

Abstract

Controlled experimental evolution during antibiotic treatment can help to explain the processes leading to antibiotic resistance in bacteria. Recently, intermittent antibiotic exposures have been shown to lead rapidly to the evolution of tolerance—that is, the ability to survive under treatment without developing resistance. However, whether tolerance delays or promotes the eventual emergence of resistance is unclear. Here we used in vitro evolution experiments to explore this question. We found that in all cases, tolerance preceded resistance. A mathematical population-genetics model showed how tolerance boosts the chances for resistance mutations to spread in the population. Thus, tolerance mutations pave the way for the rapid subsequent evolution of resistance. Preventing the evolution of tolerance may offer a new strategy for delaying the emergence of resistance.

 

Time: Tuesday, April 4, 10.00

Locale: "Darwin", 2nd floor (Ecology Building)

 

Optimal initial and adult size in animals

A few weeks ago, Erik picked a classical and highly-cited American Naturalist paper to celebrate the journal’s 150th anniversary. 

For this week’s meeting, we will read a less classical, and much less cited, paper from the treasure trove that is AmNat:

Kozlowski, J. 1996. Optimal Initial Size and Adult Size of Animals: Consequences for Macroevolution and Community Structure. The American Naturalist 147:101–114.

I’ve been reading this paper several times lately as I have been preparing my VR application. Every time, I have found it to be thought-provoking and stimulating. In the paper, Jan Kozlowski asks, using somewhat different terms, the question: what determines the number of unique adaptive peaks for body size on the macroevolutionary adaptive landscape? He does this by combining life history optimization models for optimal age and size at maturity, with models on optimal offspring size, and some really neat ecological reasoning about size-selective interactions. IThe end result is fascinating. Can’t believe this paper has only been cited 41 times! 

/Viktor Nilsson-Örtman

Where? Darwin
When? Tuesday 10.00  

There will be fika!

Abstract

Evolution of adult size and offspring size is considered with the aid of an optimal energy allocation model in which, in contrast to existing allocation models that apply a purely energetic definition of fitness, the amount of energy allocated to reproduction is divided into quanta dependent on offspring size, and net reproductive rate is maximized. This approach enables the connection between adult and offspring size to be identified: larger offspring make it optimal for their mothers to have larger adult size. Optimal offspring size exists in the range of sizes for which the ratio of production rate to mortality rate is concave upward with respect to body size. If such a range does not exist, it is optimal to produce the smallest viable offspring. Optimal adult size exists in the range of sizes for which the ratio of production rate to mortality rate is concave downward. If such a range does not exist, it is optimal to have the largest viable adults. The shape of the function representing the ratio of these two rates changes if a new size-specific predator invades the system: then, a macromutation abruptly changing either initial size or adult size can be preferred by natural selection. Possible mechanisms of such macroevolutionary changes are discussed. In the modern world, in which many small and large species with various offspring sizes exist, replacement of one species by another is expected after invasion by a size-selective predator.

Modularity: Genes, Development, and Evolution

Inspired by the discussion last week, I thought it would be nice to read a conceptual paper about the importance of modularity for evolutionary processes. If you are interested in how genetic and developmental organization shapes phenotypic evolution don't miss the next lab meeting!

Where? Darwin
When? Tuesday 10.00  

Expect fika!

 Modularity: Genes, Development, and Evolution

Diogo Melo, Arthur Porto, James M. Cheverud, and Gabriel Marroig

Abstract
Modularity has emerged as a central concept for evolutionary biology, thereby providing the field with a theory of organismal structure and variation. This theory has reframed long-standing questions and serves as a unified conceptual framework for genetics, developmental biology, and multivariate evolution. Research programs in systems biology and quantitative genetics are bridging the gap between these fields. Although this synthesis is ongoing, some major themes have emerged, and empirical evidence for modularity has become abundant. In this review, we look at modularity from a historical perspective, highlighting its meaning at different levels of biological organization and the different methods that can be used to detect it. We then explore the relationship between quantitative genetic approaches to modularity and developmental genetic studies. We conclude by investigating the dynamic relationship between modularity and the adaptive landscape and how this relationship potentially shapes evolution and can help bridge the gap between micro- and macroevolution

The Evolutionary Origins of Hierarchy, or how networks organize themselves

A few adaptationist arguments assume that organization is always a result of direct selection, so I thought it would be interesting to discuss a paper on how a few simple constraints can cause evolving systems to organize themselves regardless of what they're selected for.

As usual, Tuesday at 10:00 am in Darwin (with fika).

The Evolutionary Origins of Hierarchy

Mengistu H, Huizinga J, Mouret JB, Clune J (2016). PLOS Computational Biology 12(6): e1004829. doi: 10.1371/journal.pcbi.1004829

Hierarchical organization—the recursive composition of sub-modules—is ubiquitous in biological networks, including neural, metabolic, ecological, and genetic regulatory networks, and in human-made systems, such as large organizations and the Internet. To date, most research on hierarchy in networks has been limited to quantifying this property. However, an open, important question in evolutionary biology is why hierarchical organization evolves in the first place. It has recently been shown that modularity evolves because of the presence of a cost for network connections. Here we investigate whether such connection costs also tend to cause a hierarchical organization of such modules. In computational simulations, we find that networks without a connection cost do not evolve to be hierarchical, even when the task has a hierarchical structure. However, with a connection cost, networks evolve to be both modular and hierarchical, and these networks exhibit higher overall performance and evolvability (i.e. faster adaptation to new environments). Additional analyses confirm that hierarchy independently improves adaptability after controlling for modularity. Overall, our results suggest that the same force–the cost of connections–promotes the evolution of both hierarchy and modularity, and that these properties are important drivers of network performance and adaptability. In addition to shedding light on the emergence of hierarchy across the many domains in which it appears, these findings will also accelerate future research into evolving more complex, intelligent computational brains in the fields of artificial intelligence and robotics.

Extinction can be estimated from moderately sized molecular phylogenies

There has been some debate as to whether extinction rates can be estimated from phylogenies alone. This paper claims that it is still possible with some caveats. Even though this paper seems sort of niche, I think it is important to be caught up on this debate J. I will try to frame the debate at the beginning of the lab meeting, if some people feel lost. 

We are meeting in Darwin now Tuesday 10.00. I will bring fika. 

Link to paper. 

Tipping points in the dynamics of speciation

Hej everyone,

sorry for the late announcement, but here it comes. Let's discuss the perspective
'Tipping points in the dynamics of speciation'
in our next EXEB meeting!

As usually, Tuesday 10 am in Darwin, fika included.

Figure 1 from the paper

Patrik Nosil, Jeffrey L. Feder, Samuel M. Flaxman & Zachariah Gompert
Nature Ecology & Evolution

Speciation can be gradual or sudden and involve few or many genetic changes. Inferring the processes generating such patternsis difficult, and may require consideration of emergent and non-linear properties of speciation, such as when small changes at tipping points have large effects on differentiation. Tipping points involve positive feedback and indirect selection stemming from
associations between genomic regions, bi-stability due to effects of initial conditions and evolutionary history, and dependence on modularity of system components. These features are associated with sudden ‘regime shifts’ in other cellular, ecological, and societal systems. Thus, tools used to understand other complex systems could be fruitfully applied in speciation research.

On latent traits

For next week’s EXEB meeting we would like to discuss a paper on latent (‘White-Knight’) traits recently published in Trends in Ecology & Evolution. Latent traits are nonadaptiveOb where they originate but can become adaptive in new environments. Wherever these traits are plentiful, ecology rather than genetics might determine how fast new adaptations originate.

Fika will be provided

When: Tuesday, February 14, at 10.00

-Alexander

Title: The White-Knight Hypothesis, or Does the Environment Limit Innovations?

Link: http://dx.doi.org/10.1016/j.tree.2016.10.017

Abstract: Organisms often harbor latent traits that are byproducts of other adaptations. Such latent traits are not themselves adaptive but can become adaptive in the right environment. Here I discuss several examples of such traits. Their abundance suggests that environmental change rather than new mutations might often limit the origin of evolutionary adaptations and innovations. This is important, because environments can change much faster than new mutations arise. I introduce a conceptual model that distinguishes between mutation-limited and environment-limited trait origins and suggest how experiments could help discriminate between them. Wherever latent traits are plentiful, ecology rather than genetics might determine how fast new adaptations originate and thus how fast adaptive Darwinian evolution proceeds.

Selfing and adaptation

Posted by Jessica Abbott

Physa acuta.Taken by N yotarou.

For next week's group meeting I've chosen a paper that just came out, about the effect of self-fertilization on the rate of adaptation. We expect that in the long term, selfing depletes genetic variance. However in the short term, selfing may produce a more rapid reponse to selection. This study attempts to disentagle effects of contemporary selfing from historical selfing on the rate of adaptation, using experimental evolution in the snail Physa acuta. A commentary on this article is also avaliable here.

Title: Experimental evidence for the negative effects of self-fertilization on the adaptive potential of populations.
Abstract: Self-fertilization is widely believed to be an “evolutionary dead end”, increasing the risk of extinction and the accumulation of deleterious mutations in genomes. Strikingly, while the failure to adapt has always been central to the dead-end hypothesis, there are no quantitative genetic selection experiments comparing the response to positive selection in selfing versus outcrossing populations. Here we studied the response to selection on a morphological trait in laboratory populations of a hermaphroditic, self-fertile snail under either selfing or outcrossing. We applied both treatments to two types of populations: some having undergone frequent selfing and purged a substantial fraction of their mutation load in their recent history, and others continuously maintained under outcrossing. Populations with a history of outcrossing respond faster to selection than those that have experienced selfing. In addition, when self-fertilization occurs during selection, the response is initially fast but then rapidly slows, while outcrossing populations maintain their response throughout the experiment. This occurs irrespective of past selfing history, suggesting that high levels of inbreeding depression, contrary to expectation, do not set strong limits to the response to selection under inbreeding, at least at the timescale of a few generations. More surprisingly, phenotypic variance is consistently higher under selfing, although it quickly becomes less responsive to selection. This implies an increase in non-heritable variance, hence a breakdown of developmental canalization under selfing. Our findings provide the first empirical support of the short-term positive and long-term negative effects of selfing on adaptive potential.
When: Tuesday January 31st, at 10.00.

Sex-biased gene expression

Next week we will discuss the following paper by Cheng & Kirkpatrick for EXEB meeting:

http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1006170

"Sex specific selection and sex-biased gene expression in humans and flies"

abstract:
Sexual dimorphism results from sex-biased gene expression, which evolves when selection acts differently on males and females. While there is an intimate connection between sex-biased gene expression and sex-specific selection, few empirical studies have studied this relationship directly. Here we compare the two on a genome-wide scale in humans and flies. We find a distinctive “Twin Peaks” pattern in humans that relates the strength of sex-specific selection, quantified by genetic divergence between male and female adults at autosomal loci, to the degree of sex-biased expression. Genes with intermediate degrees of sex-biased expression show evidence of ongoing sex-specific selection, while genes with either little or completely sex-biased expression do not. This pattern apparently results from differential viability selection in males and females acting in the current generation. The Twin Peaks pattern is also found in Drosophila using a different measure of sex-specific selection acting on fertility. We develop a simple model that successfully recapitulates the Twin Peaks. Our results suggest that many genes with intermediate sex-biased expression experience ongoing sex-specific selection in humans and flies.

See you in Darwin at 10am!

Domestication syndrome in mammals

Hej hej!

Tobias will be teaching in Czech Republic next Tuesday (Jan 17), so I'm jumping the queue ;-)

I would like to discuss the following paper:

The “Domestication Syndrome” in Mammals: A Unified Explanation Based on Neural Crest Cell Behavior and Genetics

I think the authors are putting forward a very original idea that is worth while following up! In a nutshell: they suggest that a concerted response of neural crest cells is underlying the suite of traits that domesticated mammals have in common: floppy ears, smaller teeth, increased docility and tameness, curly tail, smaller brains etc.

See you in Darwin's at 10 am on Tuesday!

Abstract:

Charles Darwin, while trying to devise a general theory of heredity from the observations of animal and plant breeders, discovered that domesticated mammals possess a distinctive and unusual suite of heritable traits not seen in their wild progenitors. Some of these traits also appear in domesticated birds and fish. The origin of Darwin’s “domestication syndrome” has remained a conundrum for more than 140 years. Most explanations focus on particular traits, while neglecting others, or on the possible selective factors involved in domestication rather than the underlying developmental and genetic causes of these traits. Here, we propose that the domestication syndrome results predominantly from mild neural crest cell deficits during embryonic development. Most of the modified traits, both morphological and physiological, can be readily explained as direct consequences of such deficiencies, while other traits are explicable as indirect consequences. We first show how the hypothesis can account for the multiple, apparently unrelated traits of the syndrome and then explore its genetic dimensions and predictions, reviewing the available genetic evidence. The article concludes with a brief discussion of some genetic and developmental questions raised by the idea, along with specific predictions and experimental tests.