Showing results 221 to 240 on 1471 in total
-you can find out more about Yad's work on developmental epigenomics from her group's website:http://igfl.ens-lyon.fr/equipes/y.ghavi-helm-developmental-epigenomics
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- Évaluation et Modélisation des Effets Thérapeutiques - Bioinformatique, Phylogénie et Génomique Évolutive
Understanding how groups of species diversified, and how species phenotypes evolved during evolutionary history, is key to our understanding of patterns of biodiversity as we see them around us today. Phylogenetic comparative methods have highlighted that macroevolutionary rates (i.e. rates of diversification and phenotypic evolution) are strikingly heterogeneous in time and across lineages. However, describing and quantifying this heterogeneity, as well as understanding its drivers, remain challenging. I will present recent developments that allow a better consideration of smooth changes in diversification rates when estimating branch-specific rates across phylogenetic trees. I will also present models that allow better understanding and testing the effect of past environmental changes and interspecific interactions on diversification and phenotypic evolution. Empirical applications demonstrate the preponderance of many small (versus few important) diversification rate shifts in clades' evolution and the pervasive effect of past environmental changes on evolutionary rates across diverse clades spanning macro and microorganims.
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We consider the problem where one wants to evaluate the level of divergence between K populations. Each population is characterized by its allelic frequency prole, where allelic fre- quencies are assumed to be estimated from a sample at several (typically thousands/millions of) markers. In this context the FST is a widely used criterion for the quantication of the divergence between two populations, that can also be adapted to the question of detecting ge- nomic regions that exhibit a divergence level substantially higher than the rest of the genome. Still, the concept of FST remains ambiguous - with dierent available denitions assumed to be "connected" in some sense - and the strategy to estimate the FST when there are more than 2 populations is still an open question, the most popular strategy being to consider all possible pairs of population successively. In this presentation we will rst propose a hierarchical model for the history of population divergence and show that the two classical denitions of the FST (as provided by Hudson and Weir & Cockerham) actually measure independent quantities. We will then provide an estimation procedure based on the moment estimators suggested by Bhatia (in the case of 2 populations) and show how both the FST components and the history of population divergence may be jointly estimated. Lastly, we will consider the problem of detecting genomic regions under selection and provide a segmentation procedure for the identication of such regions. Both the estimation and the segmentation procedures will be illustrated on the 1KG human genome dataset that gathers several human populations sampled over the world.
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Symbiosis evolution is often viewed as a progress, with emergence of new adaptive properties. However, symbiosis also enhances the interdependence between partners. I describe several such interdependences, and emphasize that they arise without emergence of new property. Generally, when two partners permanently interact, a mutation in one partner can be complemented by the other. Independency is then lost without any positive selection, in a neutral evolution. The accumulation of such steps makes the reversion to independency unlikely, and drives interdependency in symbiosis.
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Age is the highest important risk factor for the most prevalent human diseases, including cancer. Telomere shortening is thought to play a central role in the aging process in humans. The link between telomeres and aging is highlighted by the fact that genetic diseases causing telomerase deficiency are associated with premature aging and increased risk of cancer. For the last two decades, this link has been investigated using long telomere mouse models. However, zebrafish has recently emerged as a powerful and complementary model system to study telomere biology. Zebrafish possess human-like telomeres that progressively decline with age. The extensive characterisation of its well-conserved molecular and cellular physiology makes this vertebrate an excellent model to unravel the underlying relationship between telomere shortening, tissue regeneration, aging and disease. In our work, we explore how telomere attrition contributes to cellular senescence, organ dysfunction, aging and disease.
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