We analyse patterns of genetic variability of populations in the presence of a large seed bank with the help of a new coalescent structure called seed bank coalescent. This ancestral process appears naturally as scaling limit of the genealogy of large populations that sustain seed banks, if the seed bank size and individual dormancy times are of the same order as the active population. Mutations appear as Poisson process on the active lineages, and potentially at reduced rate also on the dormant lineages. The presence of ‘dormant' lineages leads to qualitatively altered times to the most recent common ancestor and non-classical patterns of genetic diversity. To illustrate this we provide a Wright-Fisher model with seed bank component and mutation, motivated from recent models of microbial dormancy, whose genealogy can be described by the seed bank coalescent. Based on our coalescent model, we derive recursions for the expectation and variance of the time to most recent common ancestor, number of segregating sites, pairwise differences, and singletons. Commonly employed distance statistics, in the presence and absence of a seed bank, are compared. The effect of a seed bank on the expected site-frequency spectrum is also investigated. Our results indicate that the presence of a large seed bank considerably alters the distribution of some distance statistics, as well as the site-frequency spectrum. Thus, one should be able to detect the presence of a large seed bank in genetic data. Joint work with Bjarki Eldon, Adrián González Casanova, Noemi Kurt, Maite Wilke-Berenguer[-]

Pervasive natural selection can strongly influence observed patterns of genetic variation, but these effects remain poorly understood when multiple selected variants segregate in nearby regions of the genome. Classical population genetics fails to account for interference between linked mutations, which grows increasingly severe as the density of selected polymorphisms increases. I will describe a simple limit that emerges when interference is common, in which the fitness effects of individual mutations play a relatively minor role. Instead, similar to models of quantitative genetics, molecular evolution is determined by the variance in fitness within the population, defined over an effectively asexual segment of the genome (a "linkage block"). I will describe how we can exploit this insensitivity in a new "coarse-grained" coalescent framework, which approximates the effects of many weakly selected mutations with a smaller number of strongly selected mutations that create the same variance in fitness. This approximation generates accurate and efficient predictions for silent site variability when interference is common. However, these results suggest that there is reduced power to resolve individual selection pressures when interference is sufficiently widespread, since a broad range of parameters possess nearly identical patterns of silent site variability.[-]

In the infinitesimal model, one or several quantitative traits are described as the sum of a genetic and a non-genetic component, the first being distributed within families as a normal random variable centred at the average of the parental genetic components, and with a variance independent of the parental traits. The idea behind the normal distribution of the genetic component is that the genetic part of the trait of interest is the sum of the ‘infinitesimal' contributions of the allelic states at a very large number of loci. This model has been widely used in quantitative genetics, but less so in evolutionary biology and the precise conditionsunder which it holds has remained rather vague. In this talk, we shall provide a mathematical justification of the model as the limit as the number M of loci tends to infinity of a model with Mendelian inheritance, which includes different evolutionary processes (genetic drift, recombination, selection, mutation, population structure, ...). Generalisations of the simple version of the infinitesimal model presented here, as well as some applications, will be presented in the following talks by Nick Barton and Alison Etheridge.[-]

The reconstruction of graphical models (or networks) has become ubiquitous to analyze the rapidly expanding, information-rich data of biological or clinical interest. I will outline some network reconstruction methods and applications to large scale datasets. In particular, our group has developped information-theoretic methods and machine learning tools to infer and analyze interpretable graphical models from large scale genomics data (single cell transcriptomics, tumor expression and mutation data) as well as clinical data (analysis of medical records from breast cancer patients, Institut Curie, and from elderly patients with cognitive disorders, La Pitie-Salpetriere).[-]

Large scale biodiversity patterns result from the historical processes of speciation and extinction. In particular, the balance between speciation and extinction rates determines how species richness varies through time, across species groups, and geographical regions. Phylogenetic diversification analyses, which rely on fitting stochastic birth-death processes to phylogenetic data, can be used to estimate these macroevolutionary rates from the phylogenies of extant species, potentially further informed by paleodata. I will present recent developments that model fine-scale variations in speciation rates and that can combine neontological and paleontological evidence. Applied to empirical data, these models reveal a wide variation in speciation rates across lineages. While several models have been developed to explain these variations by differences in specific traits or abiotic and biotic conditions, models that would help us better understand the actual processes that control diversification rates are lagging behind. Speciation research at the microscale has focused on understanding the establishment of reproductive barriers, but there is increasing evidence that variations in macroevolutionary speciation rates are poorly explained by variations in the rate at which populations acquire reproductive isolation. I will present recent developments that aim at understanding i) how variations in the rates at which reproductive isolation is initiated, at which populations acquire reproductive isolation, and at which incipient species go extinct combine to explain macroevolutionary speciation rate, and ii) how population sizes, mutation rates and the mode of speciation impact this latter relationship.[-]