Do biotic forces drive long term evolution?

Posted by Beatriz Willink


Many of us are interested in understanding the links between evolutionary patterns and mechanistic processes. For next week's lab meeting I suggest a review paper on how biotic forces can drive macroevolutionary change. Looking forward to a lively discussion!

When? Next Tuesday, September 29th, 10.00
Where? Argumentet

Title: The role of biotic forces in driving macroevolution: beyond the Red Queen

Authors: Kjetil L. Voje, Øistein H. Holen, Lee Hsiang Liow, Nils Chr. Stenseth

Abstract: A multitude of hypotheses claim that abiotic factors are the main drivers of macroevolutionary change. By contrast, Van Valen's Red Queen hypothesis is often put forward as the sole representative of the view that biotic forcing is the main evolutionary driver. This imbalance of hypotheses does not reflect our current knowledge: theoretical work demonstrates the plausibility of biotically driven long-term evolution, whereas empirical work suggests a central role for biotic forcing in macroevolution. We call for a more pluralistic view of how biotic forces may drive long-term evolution that is compatible with both phenotypic stasis in the fossil record and with non-constant extinction rates. Promising avenues of research include contrasting predictions from relevant theories within ecology and macroevolution, as well as embracing both abiotic and biotic proxies while modelling long-term evolutionary data. By fitting models describing hypotheses of biotically driven macroevolution to data, we could dissect their predictions and transcend beyond pattern description, possibly narrowing the divide between our current understanding of micro- and macroevolution.

Lab meeting on assortative mating & hermaphrodites

Posted by Anna Nordén

Next week I suggest we discuss a paper about size-assortative mating induced by mate choice in simultaneous hermaphrodites. I find the meta-analysis when they compare hermaphrodites mating unilaterally or reciprocally most interesting.

Looking forward to hear what you think. See you next Tuesday (Sep 22nd), at 10 in Argumentet. Fika will be provided as usual.

Title: Size-assortative mating in simultaneous hermaphrodites: an experimental test and a meta-analysis

Abstract: Assortative mating by size has been argued to be widespread in the animal kingdom. However, the strength of size-assortative mating is known to vary considerably between species and the underlying mechanisms promoting this inter-specific variation remain largely unexplored. Size-assortative mating has been proposed to be particularly strong in simultaneous hermaphrodites, i.e. organisms that produce male and female gametes at the same time. Here, we build on this hypothesis by arguing that size-assortative mating mediated by sexual selection is generally stronger in reciprocally mating hermaphrodites compared with unilaterally mating species and separate-sexed organisms. We report a series of empirical tests suggesting that size-assortative mating in the unilaterally copulating freshwater snail Physa acuta is caused by spatial clustering of similar-sized individuals and not by mate choice. In addition, we present a meta-analysis testing, for the first time, the hypothesis that sexual selection-mediated size-assortative mating is stronger in reciprocally copulating simultaneous hermaphrodites. Overall, we found significant size-assortative mating across 18 tested species and substantial inter-specific variation. Importantly, part of this variation can be explained by mating type, providing support for the hypothesis that size-assortative mating is stronger in reciprocally mating hermaphrodites compared with unilaterally mating species. We highlight potential pitfalls when testing for sexual selection-mediated size-assortative mating and discuss the need for more experimental and comparative approaches in order to resolve the observed variation in the strength of size-assortative mating among species.

Visitors and talks this week

Hi All,

We have  a number of visitors and talks to keep in mind this week, so here is a list.

Talks

Wednesday Sep 16, 15.00 (Blå hallen)

Expanding Evolutionary Theory with Learning Theory: Implications for the Evolution of Development and Evolvability

Dr Richard Watson
University of Southampton

Friday Sep 18, 15.00 (Röda Rummet)

Evolution of haplodiploid reproduction in arthropods

Dr Laura Ross
University of Edinburgh

In addition to Richard and Laura, we are also visited by Alfredo Rago (University of Birmingham), who works on the developmental biology of sex determination in Nasonia and Daphnia, and Jarrod Hadfield (University of Edinburgh), who works on evolutionary quantitative genetics and comparative biology. Please let Tobias or Hanna know if you want to meet with any of them - we will also head to the pub on Wed (and probably Thurs too) and you are more than welcome to join.

Hope to see you all at the talks!

Lab meeting on non-adaptive plasticity and evolution of gene expression

For next week's lab meeting, let's discuss this recent Nature paper on plasticity and adaptive gene expression - topics that are of interest to many of us.

When: Sept 15, 10:00
Where: Argumentet
What: Paper discussion and Fika

Non-adaptive plasticity potentiates rapid adaptive evolution of gene expression in nature

• Cameron K. Ghalambor,
• Kim L. Hoke,
• Emily W. Ruell,
• Eva K. Fischer,
• David N. Reznick
• & Kimberly A. Hughes

Phenotypic plasticity is the capacity for an individual genotype to produce different phenotypes in response to environmental variation¹. Most traits are plastic, but the degree to which plasticity is adaptive or non-adaptive depends on whether environmentally induced phenotypes are closer or further away from the local optimum^2, 3, 4. Existing theories make conflicting predictions about whether plasticity constrains or facilitates adaptive evolution^{4, 5, 6, 7, 8, 9, 10, 11, 12}. Debate persists because few empirical studies have tested the relationship between initial plasticity and subsequent adaptive evolution in natural populations. Here we show that the direction of plasticity in gene expression is generally opposite to the direction of adaptive evolution. We experimentally transplanted Trinidadian guppies (Poecilia reticulata) adapted to living with cichlid predators to cichlid-free streams, and tested for evolutionary divergence in brain gene expression patterns after three to four generations. We find 135 transcripts that evolved parallel changes in expression within the replicated introduction populations. These changes are in the same direction exhibited in a native cichlid-free population, suggesting rapid adaptive evolution. We find 89% of these transcripts exhibited non-adaptive plastic changes in expression when the source population was reared in the absence of predators, as they are in the opposite direction to the evolved changes. By contrast, the remaining transcripts exhibiting adaptive plasticity show reduced population divergence. Furthermore, the most plastic transcripts in the source population evolved reduced plasticity in the introduction populations, suggesting strong selection against non-adaptive plasticity. These results support models predicting that adaptive plasticity constrains evolution^6, 7, 8, whereas non-adaptive plasticity potentiates evolution by increasing the strength of directional selection^11, 12. The role of non-adaptive plasticity in evolution has received relatively little attention; however, our results suggest that it may be an important mechanism that predicts evolutionary responses to new environments.

Dominance versus additivity

Posted by Jessica Abbott

X-chromosome-rated comic: The Dominant Gene, by Rather Humerus. From http://ratherhumerus.com/post/89836971148/tumblr-facebook-ratherhumerus

Sorry for being a bit late in choosing an article for next week's meeting. Don't worry, though, it's very short.

An important enterprise in genetics today is in trying to tie together molecular data with quantitative genetics. This paper uses theory to try to explain why a gene that behaves as dominant on the molecular level can still show up as part of the additive genetic variance for a trait, when investigated with quant gen.

Title: Heritability of heterozygosity offers a new way of understanding why dominant gene action contributes to additive genetic variance

Abstract: Whenever allele frequencies are unequal, nonadditive gene action contributes to additive genetic variance and therefore the resemblance between parents and offspring. The reason for this has not been easy to understand. Here, we present a new single-locus decomposition of additive genetic variance that may give greater intuition about this important result. We show that the contribution of dominant gene action to parent–offspring resemblance only depends on the degree to which the heterozygosity of parents and offspring covary. Thus, dominant gene action only contributes to additive genetic variance when heterozygosity is heritable. Under most circumstances this is the case because individuals with rare alleles are more likely to be heterozygous, and because they pass rare alleles to their offspring they also tend to have heterozygous offspring. When segregating alleles are at equal frequency there are no rare alleles, the heterozygosities of parents and offspring are uncorrelated and dominant gene action does not contribute to additive genetic variance.