Abstracts (first author)


Genetic basis of ageing evolution under differential extrinsic mortality in a nematode

Author(s): Rogell B, Chen H, Maklakov A


Ageing is inevitable in most living organisms but how ageing evolves is unclear. Because of extrinsic mortality due to a variety of biotic and abiotic factors, the strength of selection declines with age. This “selection shadow” may result in the accumulation of detrimental mutations with late-life expression or fixation of antagonistically pleiotropic mutations that increase fitness in early-life at the expense of fitness in late-life. Classic theory has thus predicted that if mortality is high, the evolutionary contribution of old individuals will be low and that this will lead to evolution of accelerated ageing and decreased longevity. However, if mortality is non-random, condition-dependent selection is likely to yield individuals with strong resistance to typical causes of mortality. Emerging theory thus suggests that condition-dependence may alter, and even reverse, the classic pattern. We have previously employed an experimental evolution design, using a nematode worm Caenorhabditis remanei, that allowed us to disentangle the effects of mortality rate (high vs low) and mortality source (random vs heat-shock) on the evolution of longevity. We observed the evolution of reduced longevity under high random mortality, confirming the classic prediction. In contrast, high condition-dependent mortality led to the evolution of increased longevity and lower late-life mortality rates, supporting a key role for mortality source in the evolution of ageing. In the present project, we examine which genes underlie the evolution of lifespan by quantifying divergences in gene expression across our selection lines. Using RNA sequencing, we quantified the differentially expressed genes in young and old nematodes from the four selection regimes. The results will be discussed.

Abstracts (coauthor)


How can sex differences arise from a largely shared genome? Theory predicts sex chromosome linkage is crucial: by reducing the intersexual genetic correlation, sex chromosomes allow males and females to evolve separately and reach their phenotypic optima. However, studies on the role of sex chromosomes and sexual dimorphism find mixed results: whereas sex chromosomes tend to harbor sex biased genes, the association between sexually dimorphic phenotypes and sex chromosomes is more tentative. We approach this question from a different perspective by examining the role of the X chromosome in the regulation of sexually dimorphic gene expression.

Using the Drosophila Genetic Reference Panel we perform a genome-wide study to find SNPs that associate with variation in sexually dimorphic gene expression. First, we find the X chromosome is a hotspot for SNPs that associate with variation in sexually dimorphic expression, particularly when SNPs are located between genes. Furthermore, we show the far reach of the X chromosome - trans-regulating SNPs that associate with variation in sexual dimorphism are more common on the X chromosome. Finally, we look in fine detail at the genomic regions with dense dimorphism-associated SNPs to see whether we can identify individual SNPs as general regulators of sexual dimorphism.

Taken together, these results suggest the X chromosome is a master regulator of sexual dimorphism and give more general insights into the genomic basis of complex phenotypes.


Chairman: Octávio S. Paulo
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XIV Congress of the European Society for Evolutionary Biology

Organization Team
Department of Animal Biology (DBA)
Faculty of Sciences of the University of Lisbon
P-1749-016 Lisbon


Computational Biology & Population Genomics Group