Abstracts (coauthor)


Because hosts and parasites exert strong selection pressure on each other, it is particularly relevant to study their interaction in an evolutionary context. Experimental Evolution permits the establishment of causality between evolutionary processes and adaptation patterns. Here we use experimental evolution of Drosophila melanogaster exposed to Drosophila C virus (DCV) to address the phenotypic and genotypic changes of hosts evolving in presence of parasites. Upon exposure to the virus, Drosophila survival increased from 33% to almost 90% after 35 generations of selection. This response carried no detectable costs in fitness in the absence of infection, and was not lost after 10 generations in the absence of selection. Cross-resistance was found for other viruses, such as CrPV and FHV, but not to bacterial pathogens. Whole genome sequencing of pooled samples of virus-selected populations and their matching controls at generation 20 uncovered two regions of significant differentiation between these groups of populations. The first corresponded to a region of 4 megabases(Mb) in the 3L chromosomal arm. This region’s peak of differentiation corresponded to a polymorphism in pastrel (pst), a gene recently associated with increased DCV resistance. The second was a pair of significantly differentiated SNPs in the X chromosome, in genes not previously associated with virus resistance. Results with a panel of deficiencies in the 3L chromosome confirmed that deficiencies which encompass pst are the ones with more influence on survival after DCV infection, in a region of approximately 2 Mb. There is ongoing work to confirm the involvement of other candidate genes in this region and of the genes in the X chromosome in resistance to DCV infection. Overall we show that selection for increased virus resistance I) is stable and bears little costs, II) is advantageous in the defense against other viral pathogens, and III) has a simple genetic basis.


Horizontally-transmitted pathogens can infect their hosts through different routes. Yet, the physiological and evolutionary consequences to the host of distinct modes of pathogen access are virtually unknown. To tackle this question, we used Experimental Evolution of Drosophila melanogaster infected with Pseudomonas entomophila by two different routes (oral and systemic). We found that adaptation to both routes relied on resistance. Moreover, adaptation to infection through one route did not protect from infection through the alternate route, indicating distinct genetic bases. Also, the two selection regimes led to markedly different evolutionary trajectories. Finally, relatively to the control population, evolved flies were not more resistant to bacteria other than Pseudomonas and showed higher susceptibility to viral infections. These specificities and trade-offs may contribute to the maintenance of genetic variation for resistance in natural populations. Moreover, our data shows that pathogen infection route affects host evolution. Therefore, the study of host-pathogen interactions should account not only on host and pathogen evolution, but also on the ecology of the infection, when interpreting patterns of variation in natural populations.


Gene duplication plays a major role in evolution of novel gene functions as it provides a material basis for variation and selection. We are interested in elucidating how cis-regulatory changes contribute to functional diversification ensuing gene duplication. To address this question we are studying the Three-Finger-Domain Protein/Ly6 gene family in insects. Members of this family encode different GPI-anchored membrane proteins and are fully conserved across drosophilids. Our analyses of the sequenced insect genomes indicate that a subset of these genes is unique to higher dipterans. We are focusing our attention on seven paralogues of Drosophila, which our phylogenetic analysis showed to derive from sequential duplications of a single orthologue. In order to determine how their expression domains diversified, we have characterized the embryonic expression patterns of the Drosophila paralogues and their unduplicated orthologues in other insects representing different phylogenetic positions and stages of duplication (the Mediterranean fruit fly, Ceratitis capitata, the scuttle fly, Megaselia abdita, the mosquito, Anopheles, the butterfly, Bicyclus anynana and the red flour beetle, Tribolium castaneum). We found that the original expression domain of the unduplicated orthologue localized predominantly to the developing nervous system, which, upon subsequent duplications, expanded to a wide array of tissues. While a subset of the duplicates retained the tissue-specificity of the unduplicated orthologues, the others acquired novel tissue-specific expression suggesting neofunctionalization. We are currently identifying the cis-regulatory elements of the duplicates and the unduplicated orthologues to elucidate the cis-regulatory mechanisms underlying the evolution of divergent expression patterns.


The insect ovary consists of parallel repetitive units called the ovarioles, which are assembly lines for the production of eggs. The number of ovarioles is positively correlated with egg production rate and therefore is a morphological trait closely related to fitness. Interestingly, ovariole number exhibits both developmental plasticity and interspecific variation among Drosophila species. These two features of ovariole number provide an opportunity to investigate the contribution of developmental plasticity in evolutionary processes. To address this challenge, our approach is to compare the developmental mechanisms underlying the plastic response with those underlying genetic differences between related species. Here, we discuss how plasticity in ovariole number is regulated in Drosophila melanogaster. Since ovariole number is determined during larval development, we first described how nutrition affects this reproductive trait in carefully staged larvae. Our analysis revealed that early third instar larvae fed on sucrose alone show a stronger reduction in ovariole number than later stages, suggesting an early nutrition-dependent mechanism for ovariole formation. Further, we found that larvae fed on sucrose alone early in the third instar had ovaries with a reduced number of dividing somatic cells. Moreover, they show a delay in the onset of differentiation of the terminal filament cells, which serve as the starting point for ovariole formation. Currently, we are manipulating insulin and ecdysone signalling in the terminal filament precursors to determine the role of each in regulating the proliferation and differentiation of these cells to generate plasticity in ovariole number. This powerful approach will shape our understanding of how the environment creates phenotypic variation through changes in development and ultimately how environmentally-induced variation impacts evolutionary diversification.


Chairman: Octávio S. Paulo
Tel: 00 351 217500614 direct
Tel: 00 351 217500000 ext22359
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email: mail@eseb2013.com


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