European Society for Evolutionary Biology ORAL PRESENTATION ABSTRACTS AND LIST OF POSTERS 14th Congress, Lisbon, Portugal, 19 - 24 August 2013 Symposia 1. Experimental Evolution on Empirical Fitness Landscapes 13 2. Selection and Evolution in Natural Populations 40 3. Molecular Evolutionary Innovations 131 4. Evolution of Symbiotic Interactions in Communities: Novel Approaches 162 5. Phenotypic Plasticity: Mechanisms, Ecology and Evolution 206 6. Evolutionary Consequences of an Early Germ-Soma Segregation 306 7. The Nature and Mechanisms of Evolution of Species Recognition Systems 317 8. Evolutionary Significance of Epigenetic Variation 338 9. Genetics and Genomics of Host-Parasite Coevolution 354 10. Genomics and Experimental Evolution 424 11. Advances in Quantitative Approaches to Recent Evolutionary Change in Humans 459 12. Studying Multigene-Family Evolution in the Post-Genomic Era: Towards a Population Genomic Approach to MHC Evolution 483 13. Rapid Evolution and Population Genetics 508 14. Non Genetic Inheritance 564 15. Attack and Defense: Evolutionary and Ecological Consequences of Individual Variation 587 16. Evolutionary Biology in China 653 17. Linking Genome Evolution at Different Time Scales 666 18. Evolutionary Demography 701 19. Evolutionary Consequences of Deception 742 20. Mechanisms of Trade-offs 760 21. The Evolution and Maintenance of Heritable Colour Polymorphsims: from Ecology to Genomes 808 22. The Evolution and Genetics of Drug Resistance 835 23. Genomic Islands: Their Role in Adaptation and Speciation 873 24. Unifying Paleobiologiccal and Comparative Perspectives on Character Evolution 934 25. New Directions in Sex Role Research 952 26. The Genomic Architecture of Adaptive Traits: do QTNS Generally Exist? 999 27. Evolutionary Conservation: the Applied Side of Evolutionary Biology 1021 28. Non-Genetic Transfer of Immunity Across Generations – Evolution and Underlying Mechanisms 1080 29. Actively Learning Evolution: Methods and Resources 1099 30. Phylogenetics and Phylogeography 1109 31. Development, Behaviour and Evolution 1254 32. Climate Change and Evolution 1324 33. Population Ecology 1370 34. General Symposium 1440 Plenary Lectures 1. Tuesday August 20 Juliette De-Meaux, University of Münster, Germany “The molecular underpinnings of adaptation in Arabidopsis thaliana” 2. Wednesday August 21 Dieter Ebert, University of Basel, Switzerland “Population genetics of host-parasite coevolution” 3. Thursday August 22 Mel Greaves, The Institute of Cancer Research, United Kingdom “Cancer through the eye of evolutionary medicine” 4. Friday August 23 Trudy Mackay, North Carolina State University, United States “Charting the Genotype-Phenotype map: Lessons from Drosophila” 5. Saturday August 24 Virpi Lummaa, University of Sheffield, United Kingdom “Sex differences in natural selection on reproductive scheduling and longevity in humans” PRESIDENTIAL ADDRESS Roger Butlin, University of Sheffield, United Kingdom “Reinforcement (and other modes of speciation)” JOHN MAYNARD SMITH PRIZE LECTURE Richard FitzJohn, Macquarie University, Australia “What drives biological diversification? Detecting traits under species selection” DISTINGUISHED FELLOW LECTURE Rolf Hoekstra, Wageningen University, Netherlands “♀ ♂ + -” 4 Plenary (Tue 20) THE MOLECULAR UNDERPINNINGS OF ADAPTATION IN ARABIDOPSIS THALIANA Juliette De-Meaux1 1Westfälische Wilhelms-Universität, Germany [email protected] The theories used in Evolutionary Biology are rooted in powerful concepts, most of which were constructed before the discovery of DNA. In the meantime, we understand much better how function is encoded in the genome. The current task is now to examine how genetic modifications in molecular systems can promote adaptation in natural populations. Arabidopsis thaliana is a focal system in plant molecular biology. Genes and pathways controlling its development, physiology and immunity have been researched intensively. Its broad latitudinal distribution in Europe makes it a unique system to dissect the molecular underpinnings of adaptation. I will review some of the molecular changes that have been successfully associated with adaptive evolution in A. thaliana. I will thereby illustrate why reconciling molecular and evolutionary biology is a difficult yet necessary task, requiring a shift of concepts in both molecular biology and evolutionary theory. 5 Plenary (Wed 21) POPULATION GENETICS OF HOST-PARASITE COEVOLUTION Dieter Ebert1 1Zoological Institute, University of Basel, Switzerland [email protected] Hosts evolve to minimize the fitness reduction caused by parasites, while parasites optimise the exploitation of their hosts. In models of this process high genetic specificity in host – parasite interactions is assumed. These interactions are in the centre of theory of host – parasite coevolution and determine important aspects of the coevolutionary process, such as its tempo and mode, the occurrence of cyclic allele frequencies, and the potential for evolutionary novelty. They are also crucial for the consequences of coevolution, such as the maintenance of sex and of genetic variation. In my presentation I will analyse the genetic architecture of host-parasite interactions and will test predictions and assumptions of models of host – parasite coevolution. Finally I will match predictions with patterns from long-term coevolution records. 6 Plenary (Thu 22) CANCER THROUGH THE EYE OF EVOLUTIONARY MEDICINE Mel Greaves1 1Division of Molecular Pathology, The Institute of Cancer Research, United Kingdom [email protected] There are two striking examples of somatic cell evolution in humans (and vertebrates in general): the immune system and cancer. In the former, recombinase enzymes target diversification of the immunoglobulin and T cell receptor loci in lymphocytes provides the substrate (>1011 variants) for natural selection by infectious antigenic epitopes. In cancer, stochastic mutational processes drive genetic diversification of clones of cell that under natural selection within complex tissue ecosystems and in response to therapeutic pressure. Starting from a single founder cell, cancer clones evolve over time frames of 1 to 50 years, often in a covert fashion, but the end result is the generation of a robust and weed-like quasi-species of immortal and invasive cells that hijack normal tissue function. In exceptional circumstances, cancer cells transit, parasitic like, individual to individual. Therapy itself inadvertently provides positive selective pressure for the emergence of drug-resistant mutant sub- clones. Whole genome sequencing reveals the extent of genetic, mutational complexity in cancer and when interrogated at the single cell level, it is clear that cancers have tree-like clonal phylogenies with variegated genetics of sub-clones. Within sub-clones, cells with stem cell properties sustain and propel clonal expansion and provide the cellular units of selection. Cancer’s Darwinian character has substantial implications for prevention, prognosis and treatment. 7 Plenary (Fri 23) CHARTING THE GENOTYPE-PHENOTYPE MAP: LESSONS FROM DROSOPHILA Trudy Mackay1 1Department of Genetics, North Carolina State University, United States [email protected] Quantitative traits are affected by multiple interacting loci with individually small and environmentally sensitive effects. Knowledge of the detailed genetic architecture of quantitative traits is important from the perspectives of evolutionary biology, human health and plant and animal breeding. Understanding the genetic architecture of quantitative traits begins with identifying the genes regulating these traits, mapping the subset of genetically varying quantitative trait loci (QTLs) in natural populations, and pinpointing the molecular polymorphisms defining QTL alleles. Drosophila brings an impressive toolkit to the challenge of genetically dissecting quantitative traits. I will discuss insights into the complex genetic architecture of quantitative traits obtained from genome wide association mapping in the Drosophila melanogaster Genetic Reference Panel (DGRP), which consists of 192 sequenced inbred lines derived from the Raleigh, USA population. These studies indicate that epistatic gene action is common, and additivity can be an emergent property of underlying genetic interaction networks. Epistasis causes hidden quantitative genetic variation in natural populations, the potential for rapid speciation, and negatively impacts the predictive ability of additive models. These observations offer valuable lessons for understanding the genetic basis of variation for quantitative traits in other organisms. 8 Plenary (Sat 24) SEX DIFFERENCES IN NATURAL SELECTION ON REPRODUCTIVE SCHEDULING AND LONGEVITY IN HUMANS Virpi Lummaa1 1Department of Animal and Plant Sciences, University of Sheffield, United Kingdom [email protected] Despite senescence with age, most animals retain ability to reproduce until relatively close to death. Humans provide an interesting case because with mid-life menopause, women show a radical de- coupling of senescence in reproductive and somatic systems, leading to up to half of total lifespan spent post-reproductive. By contrast, men maintain reproductive ability until much later ages. Although men thus sire offspring at older ages than women, nearly all contemporary human populations exhibit sexual dimorphism in lifespan with women outliving men by on average of five years. While proximate causes for such fertility and lifespan differences