Invited speakers
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Wiesław Babik Jagiellonian University in Krakow |
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I use information from DNA sequences to infer history of populations. In particular I am interested in the causes, demography and the age of intraspecific differentiation and divergence between closely related species, as well as in studying the extent of gene flow between diverging populations. Fundamental problems in evolutionary biology include questions how populations diverge over space and time and whether speciation with gene flow has been a common phenomenon. Quantitative answers may be provided by studying, within coalescent framework, genealogies of multiple genomic regions in many population/species pairs. I will discuss methods that reconstruct the history of gene flow between diverging populations and the most important insights obtained from the application of these methods. Multiple sequence markers sampled across genome enable both averaging out the stochastic effects of the coalescent process and taking into account the possibility that various genomic regions encountered different histories of introgression and gene flow between diverging populations. Such heterogeneity is consistent with the view that reproductive isolation may build up gradually across genome, with some genomic regions becoming effectively isolated earlier than others. Methods reconstructing the temporal distribution of gene flow bring the promise of the quantitative assessment of frequency and patterns of differentiation with gene flow in nature. It is however extremely important to understand the effects of violation of model assumptions on the accuracy of inference. I will suggest how next generation sequencing technologies may speed up multilocus studies of population divergence facilitating the high throughput development and analysis of multiple sequence markers for virtually any organism.
Topic for discussion: How confident should we be about estimates of historical gene flow derived from multilocus studies? |
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Zoltan Barta University of Debrecen |
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Among recent research interest of Zoltan Barta are:
Many animals live together forming groups ranging in size from two (caring parents) to thousands of individuals (sea birds breeding colonies). Group living offers tremendous possibilities for social interactions. At one end of the range of interactions are, for instance, the infanticide committed by common marmosets females, or the cannibalism of chicks in herring gull colonies. Less extreme forms of conflict include stealing of nest material from neighbouring nests or the exploitation of other food finding effort. Moving further towards the other end of the spectra we pass behaviours like biparental care, contribution to the group effort of vigilance or cooperative hunting of lions. At the other extreme behaviours like eusociality or human society can be found. In order to understand this variation in social behaviour several models were proposed but most of them neglected the internal state of the animals. We do, however, know that the internal state is important. There are large differences between the behaviour of a hungry and a well-fed animal. A dominant behaves rather differently than a subordinate. Applying testosterone implants can change behaviour dramatically. What is unclear how including internal state change the models of conflict and cooperation. Through several case studies I will explore this issue and show that the incorporation of state can change the outcome of models significantly. Topic for discussion: Modelling optimal behaviour over the annual cycle McNamara J.M. & Houston A.I. 2008. Optimal annual routines: behaviour in the context of physiology and ecology. Phil. Trans. R. Soc. B 363: 301 - 319 Barta Z., McNamara J.M., Houston A.I., Weber T.P., Hedenstrom A. & Fero O. 2008. Optimal moult strategies in migratory birds. Phil. Trans R Soc. Lond. B 363: 211 - 229 |
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Sinead Collins University of Edinburgh |
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I use experimental evolution in the unicellular alga Chlamydomonas, along with studies of analogous natural microalgal populations, to study how classical adaptive processes (selective sweeps, adaptive walks) are affected by environmental complexity. Complex environments may be those that change at different rates (glacial-interglacial cycles vs the current rate of global change), that involve many concurrent changes (changes in temperature and light levels and carbon levels), or that involve changes in competition and adaptation at the same time (changes in the species composition of communities on the same timescale as the evolution of a given species). Many aspects of this work are used, either in models or in collaborative experiments using marine algae, to understand better how phytoplankton populations may respond to global change. The process of adaptation is so fundamental to our understanding of biology that it has been studied intensively for over 150 years. We now have such a clear picture of adaptation in simple environments that we can predict the timing and magnitude of fitness increases in large evolving populations and confirm these predictions by experimental evolution in laboratories. We also understand how fluctuating environments or constant environmental change systematically affects adaptation, including speeding up or slowing down rates of environmental change. However, environmental change in the real world is anything but simple, and it is often unclear what results from simple laboratory systems tell us about adaptation outside the lab. I will discuss empirical and modelling work that extends our basic understanding of adaptation by explaining how ecological factors, such as different rates of environmental change, or the presence of competitors, can systematically affect adaptive walks. The problem of integrating complex ecological factors into our standard “adaptive walk” metaphor is not only an interesting exercise. I will also explore how this affects our ability to understand the specific case of how marine phytoplankton may respond to global change over hundreds or thousands of generations.
Topic for discussion: Since the 1930s , we have considered adaptation from de novo mutation in the case where a population is placed suddenly in an environment to which it is poorly adapted, and where fitness increases while the environment remains constant (think RA Fisher). However, natural environments rarely remain constant. One notable instance of a continuously changing environment is global change, where temperatures and CO2 concentrations are increasing on average, and will continue to increase in the foreseeable future. For adapting populations, this represents a "moving optimum". How does adapting to a moving optimum affect the size and timing of fixed mutations (or fitness increases)? How might this insight affect standard population genetics tests for selective sweeps? Does considering adaptation towards a moving optimum represent a significant shift in how we think about and detect adaptation, or is it just fine-tuning what we already know? |
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Ellen Decaestecker Katholieke Universiteit Leuven |
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Host-parasite interactions are a key structuring force in ecosystems, driving coevolution. We study the evolutionary ecology of host-parasite interactions by using the water flea Daphnia and its parasites as a model. The omnipresence of Daphnia parasites in combination with their short generation time and their virulence effects, enable parasites to reduce Daphnia population density and to influence Daphnia population genetic structure. In their “arms race” against the fast evolving parasites, there will be selection and evolution in the Daphnia. Daphnia and its parasites provide an unique possibility to study long-term coevolutionary processes, as both Daphnia and its parasites produce dormant stages, which are conserved in layered pond sediments. This reflects an archive of past evolutionary dynamics in a natural system. Further, we investigate how the biotic and abiotic environment influences defences against parasites. In first instance, we focus on trade-offs in defences between multiple enemies as trade-offs between predator and microparasite avoidance are important in the evolution of habitat selection behavior in Daphnia. Secondly, we investigate how host-parasite dynamics are influenced by changing (eutrophication, pollution and climate change) environments. At last, we investigate the interaction between host-parasite coevolution and metacommunity processes in a spatial context. Fast evolving parasites are a key structuring force in host ecosystems. In their 'arms race' with fast evolving parasites, there will be selection in Daphnia populations against defense mechanisms that are abundant in the momentary interaction, as parasites adapt to the most abundant host genotypes. The resulting antagonism produces an ongoing co-evolutionary dynamic that maintains genetic variation in infectivity traits. It is, however, notoriously difficult to study co-evolutionary dynamics in nature, because time series over many generations are needed. Consequently, empirical evidence for the process of host-parasite co-evolution in natural systems is lacking. To obtain insight in the fundamental processes that drive the co-evolutionary dynamics of antagonistic host-parasite interactions, the water flea Daphnia and its parasites were used as an evolutionary and experimental model. A historical reconstruction of a natural Daphnia-parasite interaction was realized using what amounts to a time machine in a shallow pond, as this pond contains layered sediments with both Daphnia resting eggs and spores of her bacterial parasites. These resting stages remain dormant for many years, but can be revived and thus provide an archive of past evolutionary dynamics in a natural system. Our results revealed Red Queen host-parasite dynamics. These specific host-parasite interactions are further investigated in a wider ecological framework investigating the link of these interactions with defenses towards predation and dynamic environments. Articles for discussion: Urban et al. 2008. The evolutionary ecology of metacommunities. TREE 23: 311-317 |
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Paweł Golik University of Warsaw |
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Currently I work at the Department of Genetics and Biotechnology of the University of Warsaw, Poland. Since 2008 I’m the vice-director of the Institute. Between 2000 and 2002 I worked as a post-doc at Doug Wallace's lab at Emory University in Atlanta, Georgia, USA. I studied biology at the Warsaw University, getting my M.Sc. in Molecular Biology in 1993.I did my Ph.D thesis in a joint research project between Department of Genetics and Centre de Génétique Moléculaire in Gif-sur-Yvette, France. I worked on nuclear genes controlling RNA degradation in yeast mitochondria. I received my Ph.D. in Warsaw in 1999. Pentatricopeptide repeat (PPR) proteins form the largest known RNA-binding protein family and are found in all eukaryotes, being particularly abundant in higher plants. PPR proteins localize mostly in mitochondria and chloroplasts, where they modulate organellar genome expression on the posttranscriptional level. In our lab we described the function of Dmr1p – one of the PPR proteins of S.cerevisiae, and found it to be essential for the stability of the mitochondrial genetic system. We also developed a new in silico approach that allowed us to identify the PPR motifs in proteins encoded by the genomes of different yeast species. Combining the results of comparative sequence analysis with data obtained from genetic experiments gives new insights into the rapid divergent evolution of the PPR family, and allows us to speculate on the evolutionary consequences of some systems-level properties of mitochondria. Topic for discussion: Why do we still have a mitochondrial genome?
The mitochondrial genome is an evolutionary relic of the eubacterial ancestry of these organelles. In the course of reductive evolution the organellar genome underwent a very significant reduction, with the majority of the mitochondrial proteome being now encoded in the nucleus. The situation observed in modern Eukaryotes, where the mitochondrial DNA encodes only a handful of proteins, yet hundreds of nuclear-encoded factors are required for its maintenance and replication, appears to be absurd and begets the question, why the reduction of mtDNA was not completed and why the costly maintenance of this evolutionary relic seems to be still required. Possible explanations range from simple mechanistic answers to complex evolutionary arguments. |
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Massimo Pigliucci City University of New York |
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Prof. Pigliucci has a Doctorate in Genetics from the University of Ferrara (Italy), a PhD in Evolutionary Biology from the University of Connecticut, and a PhD in Philosophy from the University of Tennessee. He has done post-doctoral research in evolutionary ecology at Brown University and is currently Professor of Philosophy at the City University of New York. His research interests include the philosophy of biology, in particular the structure and foundations of evolutionary theory, the relationship between science and philosophy, and the relationship between science and religion. Prof. Pigliucci is the Editor-in-Chief of the open access journal Philosophy & Theory in Biology (philosophyandtheoryinbiology.org). He has been elected fellow of the American Association for the Advancement of Science “for fundamental studies of genotype by environmental interactions and for public defense of evolutionary biology from pseudoscientific attack.” In the area of public outreach, Prof. Pigliucci has published in national magazines such as Skeptic, Skeptical Inquirer, Philosophy Now, The Philosopher’s Magazine, Secular Nation and American Atheist magazine. He has also been elected a Fellow of the Committee for Skeptical Inquiry. Pigliucci pens the “Rationally Speaking” blog (rationallyspeaking.org), hosts the podcast by the same name, and publishes the “5-minute Philosopher” videos on YouTube. Title of talk: Toward an Extended Evolutionary Synthesis? Abstract: Modern evolutionary biology began with the publication of Charles Darwin’s Origin of Species in 1859. Since then, two major reassessments of the theory have taken place: the neo-Darwinian turn at the end of the 19th century (which definitely excluded Lamarckism), and the Modern Synthesis of the 1930s and ‘40s (which reconciled Mendelism, statistical genetics and Darwinism). For years now scholars have been hinting at the necessity of a new Extended Synthesis, building on the conceptual framework laid out during the middle of the 20th century while incorporating new empirical findings and theoretical advances that have occurred since. In this talk I sketch how an Extended Synthesis is beginning to shape, with contributions from fields such as evo-devo, genomics, ecology and complexity theory, and with the incorporation of new concepts like phenotypic plasticity, modularity and evolvability. This makes for much intellectual excitement, not to mention some elementary observation on the sociology and psychology of science. Topic for discussion: as above Articles: Müller G.B. 2007. Evo–devo: extending the evolutionary synthesis. Nature Reviews Genetics 8: 943-949 Pigliucci M. 2009. An Extended Synthesis for Evolutionary Biology. The Year in Evolutionary Biology 2009: Ann. N.Y. Acad. Sci. 1168: 218–228 |
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Jacek Radwan Jagiellonian University in Krakow |
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Research of my team focuses on sexual selection, its evolutionary-genetic background and implications for conservation. I'm interested in developing strong tests of good genes models of sexual selection, which requires understanding mechanisms maintaining genetic variance for fitness. Mutations and genes interacting with parasites, such as MHC genes, are important sources of genetic variation, therefore I study their role in sexual selection. I also investigate the role of sexual selection and MHC genes in biological conservation. “Good genes” models of sexual selection assume that populations maintain additive genetic variance for fitness, and that competition of sexual partners is won by individuals with higher breeding values for fitness. The “good genes” theory was developed to explain evolution of female preferences for elaborate sexual traits, which, being costly to produce and/or maintain, are likely to be afforded only by males in good condition, which should be males with high breeding value for fitness. Choosy females can thus accrue genetic benefit in terms of improved progeny fitness. The theory has also implication of the evolution of sexual reproduction, because “good genes” mechanism should increase fitness of sexual populations compared to asexual ones, thus compensating for the “twofold cost of sex”. In particular, sexual selection was predicted to purge populations of deleterious mutations, continuous influx of which is thought to be one of the main sources of VA for fitness in natural populations. I will present recent experimental tests of this prediction, including examples from my own research.
Topic for discussion: How do preferences for sexual traits evolve? Are such preference associated with genetic benefits? What are the ways to test this? |
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Andrew F. Russell University of Exeter National Center for Scientific Research, Moulis |
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Cooperative behaviour appears to conflict with
Cooperative breeding systems, wherein individuals provide care to the offspring of others, appear to counter current evolutionary thinking. Such paradoxical breeding systems are suggested to evolve when constraints on independent Russell A.F. & Lummaa V. 2009. Maternal effects in cooperative breeders: from hymenopterans to humans. Phil. Trans. R. Soc. B 364: 1143-1167
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Isaac Salazar-Ciudad Autonomous University of Barcelona |
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I am senior researcher on the mechanisms of evolution. My focus is on morphological evolution and to this end I have been developing theories about the interdependence between the dynamics of development and the dynamics of evolution. This has brought me to study the mechanisms of pattern formation in development that are responsible for the generation of phenotypic variation in populations. Thus, my aim is to understand the multiple types of relationships between genetic (and environmental) variation and morphological variation in different animal species and their effects on evolution. In practice my work involves integrating experimental data in developmental biology into mathematical models of development and evolution. Title of talk: Why should we care about theoretical evo-devo? There is a relatively sharp divide among evolutionary biologists. Roughly speaking there are those that consider that understanding the mechanisms of embryonic development would not dramatically change current evolutionary theory (roughly the neo-Darwinian paradigm) and those that do. In this talk I would present work by me and others that shows that the first view is simply untenable. First, I would analyze how different subfields have a completely different view about which questions evolutionary biology is aiming at. Second, I will indicate some assumptions implicit in the neo-Darwinian paradigm that preclude it to give satisfactory answers to both sets of questions. All those relate to the phenotypic variation possible in each generation and to the relationship between genetic and phenotypic variation. Third, I will explain how some of these questions can be approached from evo-devo. I will put specific examples of this latter approaches from my own work. I will finish with a brief discussion about how this kind of approaches can lead to a more predictive evolutionary theory. Topic for discussion: as above For most of the last century development has somehow been left out of mainstream evolutionary biology. Populational genetics, and to a lesser extent populational ecology, has been perceived as the field at the core of the theoretical foundations of evolutionary theory. A prominent research topic, from this perspective, has been the dynamics of adaptation. This is, which factors (populational, ecological, etc...) affect the speed of adaptation. The question of the direction of evolutionary change has received less direct attention. That is, in which specific way the phenotype changes in each generation. Classically, it is stated that there is additive genetic variation for most traits and that thus the direction of evolutionary change depends on the direction of selective pressures. The evo-devo field of research arose as an opposition to that. From this perspective we cannot assume what the variation is (as “there is additive genetic variation in most traits”), because that is determined by development (since development is the mechanisms by which genetic variation gives rise to specific phenotypic variation). Thus development is crucial to understand the direction of evolutionary change. Possible questions for discussion are:
Salazar-Ciudad I., Jernvall J.A. 2010. Computational model of teeth and the developmental origins of morphological variation. Nature 464:583-6 |
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Marta Szulkin University of Oxford |
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My interests lie in evolutionary biology, ecology and conservation genetics. I aim to improve our understanding of how different aspects of additive and non-additive gene action shape the phenotype, particularly so in natural populations. I have a broad interest in using any animal taxa as model system, although I am currently focusing on wild population of birds (Paridae) and mammals (Ursidae). My present and future investigations include the following: Non-additive genetic effects
Quantitative genetics of the brown bear (Ursus arctos) Recent man-made environmental change poses great challenges to the maintenance of adequate genetic diversity across a large array of plant and animal taxa. In the same time, genetic diversity is essential to adapt to a changing world. It has now become pivotal to not only understand the key elements threatening the persistence of species, but also to remediate and avoid further genetic depletion. Using vertebrate species as case studies, I discuss the main drivers influencing levels of genetic diversity, and ask how these can be inferred and incorporated in conservation genetics management. I then address the question of why including evolutionary biology to conservation planning is important if species survival is a long-term conservation focus. Topic for discussion: What does it take for a species to make it to the 22nd century?
Mace G.M. & Purvis A. 2008. Evolutionary biology and practical conservation: bridging a widening gap. Molecular Ecology 17:9-19. |
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