Rising out of the ashes: additive genetic variation for susceptibility to Hymenoscyphus fraxineus in Fraxinus excelsior

Facundo Muñoz, Benoit Marçais, Jean Dufour, Arnaud Dowkiw

Environmental unpredictability and inbreeding depression select for mixed dispersal syndromes

Environmental unpredictability and inbreeding depression select for mixed dispersal syndromes
Jorge Hidalgo, Rafael Rubio de Casas, Miguel A. Munoz

Mixed dispersal syndromes have historically been regarded as bet-hedging mechanisms that enhance survival in unpredictable environments, ensuring that some propagules stay in the maternal environment while others can potentially colonize new sites. However, this entails paying the costs of both dispersal and non-dispersal. Propagules that disperse are likely to encounter unfavorable conditions for establishment, while non-dispersing propagules might form populations of close relatives burdened with inbreeding. Here, we investigate the conditions under which mixed dispersal syndromes emerge and are evolutionarily stable, taking into account the risks of both environmental unpredictability and inbreeding. Using mathematical and computational modeling we show that high dispersal propensity is favored whenever temporal environmental unpredictability is low and inbreeding depression high, whereas mixed dispersal syndromes are adaptive under conditions of high environmental unpredictability, but more particularly if also inbreeding depression is small. Although pure dispersers can be selected for under some circumstances, mixed dispersal provides the optimal strategy under most parameterizations of our models, indicating that this strategy is likely to be favored under a wide variety of conditions. Furthermore, populations exhibiting any single phenotype go inevitably extinct when environmental and genetic costs are high, whilst mixed strategies can maintain viable populations even under such conditions. Our models support the hypothesis that the interplay between inbreeding depression and environmental unpredictability shapes dispersal syndromes, often resulting in mixed strategies. Moreover, mixed dispersal seems to facilitate persistence whenever conditions are critical or nearly critical for survival.

Toy model for the adaptive origins of the sexual orientation continuum

Toy model for the adaptive origins of the sexual orientation continuum
Brian Skinner

Same-sex sexual behavior is ubiquitous in the animal kingdom, but its adaptive origins remain a prominent puzzle. Here I suggest the possibility that same-sex sexual behavior arises as a consequence of the competition between an evolutionary drive for a wide diversity in traits, which improves the adaptability of a species, and a drive for sexual dichotomization of traits, which promotes opposite-sex attraction and increases the rate of reproduction. A simple analytical “toy model” is proposed for describing this tradeoff. The model exhibits a number of interesting features, and suggests a simple mathematical form for describing the sexual orientation continuum.

Automatic and accurate identification of integrons and cassette arrays in bacterial genomes reveals unexpected patterns

Automatic and accurate identification of integrons and cassette arrays in bacterial genomes reveals unexpected patterns

Jean Cury, Thomas Jové, Marie Touchon, Bertrand Néron, Eduardo PC Rocha

Agent based models to investigate cooperation between cancer cells

Agent based models to investigate cooperation between cancer cells

Joao Xavier, William Chang

Exact numerical calculation of fixation probability and time on graphs

Exact numerical calculation of fixation probability and time on graphs
Laura Hindersin, Marius Möller, Arne Traulsen, Benedikt Bauer

The Moran process on graphs is an interesting model to study the spread of a new mutant in a spatially structured population. Exact analytical solutions for the fixation probability and time have been found for only a few classes of graphs so far. Simulations are time-expensive and many realizations are necessary, as the variance of the fixation times is high. We present an algorithm that numerically computes these quantities by an approach based on the transition matrix. The advantage over simulations is that the calculation has to be executed only once. Building the transition matrix is automated by our algorithm. This enables a fast and interactive study of different graph structures and their effect on fixation probability and time. We provide a fast implementation in C with this note. Our code is very flexible, as it can handle two different update mechanisms (Birth-death or death-Birth), as well as directed or undirected graphs.

On the importance of being structured: instantaneous coalescence rates and a re-evaluation of human evolution

On the importance of being structured: instantaneous coalescence rates and a re-evaluation of human evolution
Olivier Mazet, Willy Rodríguez, Simona Grusea, Simon Boitard, Lounès Chikhi

Most species are structured and influenced by processes that either increased or reduced gene flow between populations. However, most population genetic inference methods ignore population structure and reconstruct a history characterized by population size changes under the assumption that species behave as panmictic units. This is potentially problematic since population structure can generate spurious signals of population size change. Moreover, when the model assumed for demographic inference is misspecified, genomic data will likely increase the precision of misleading if not meaningless parameters. In a context of model uncertainty (panmixia \textit{versus} structure) genomic data may thus not necessarily lead to improved statistical inference.
We consider two haploid genomes and develop a theory which explains why any demographic model (with or without population size changes) will necessarily be interpreted as a series of changes in population size by inference methods ignoring structure. We introduce a new parameter, the IICR (inverse instantaneous coalescence rate), and show that it is equivalent to a population size only in panmictic models, and mostly misleading for structured models. We argue that this general issue affects all population genetics methods ignoring population structure. We take the PSMC method as an example and show that it infers population size changes that never took place. We apply our approach to human genomic data and find a reduction in gene flow at the start of the Pleistocene, a major increase throughout the Middle-Pleistocene, and an abrupt disconnection preceding the emergence of modern humans.

Negative selection maintains transcription factor binding motifs in human cancer

Negative selection maintains transcription factor binding motifs in human cancer
I. E. Vorontsov, I. V. Kulakovskiy, G. Khimulya, E. N. Lukianova, D. D. Nikolaeva, I. A. Eliseeva, V. J. Makeev

Somatic mutations in cancer cells affect various genomic elements disrupting important cell functions. In particular, mutations in DNA binding sites recognized by transcription factors can alter regulator binding affinities and expression of target genes. A number of promoter mutations have been linked with an increased risk of cancer, mutations in binding sites of selected transcription factors have been found under positive selection. However, negative selection of mutations in coding regions is elusive and significance of negative selection in non-coding regions remains controversial.
Here we present analysis of transcription factors with binding sites co-localized with non-coding variants. To avoid statistical bias we account for mutation signatures of different cancer types. For many transcription factors, including multiple members of FOX, HOX, and NR families, we show that human cancers accumulate fewer mutations than expected by chance that increase or decrease affinity of binding motifs. Such conservation of motifs is even more exhibited in DNase accessible regions.
Our data demonstrate negative selection against binding sites alterations and suggest that this selection pressure protects cancer cells from rewiring of regulatory circuits. Further analysis of transcription factors and the respective conserved binding motifs can reveal cell regulatory pathways crucial for the survivability of various human cancers.

Evolutionary history of the global emergence of the Escherichia coli epidemic clone ST131

Evolutionary history of the global emergence of the Escherichia coli epidemic clone ST131

Nicole Stoesser, Anna Sheppard, Louise Pankhurst, Nicola de Maio, Catrin E Moore, Robert Sebra, Paul Turner, Luke W Anson, Andrew Kasarskis, Elizabeth M Batty, Veronica Kos, Daniel J Wilson, Rattanaphone Phetsouvanh, David Wyllie, Evgeni Sokurenko, Amee R Manges, Timothy J Johnson, Lance B Price, Timothy E. A. Peto, James R Johnson, Xavier Didelot, Ann Sarah Walker, Derrick W Crook, Modernising Medical Microbiology Informatics Group

Strongly asymmetric hybridization barriers shape the origin of a new polyploid species and its hybrid ancestor

Strongly asymmetric hybridization barriers shape the origin of a new polyploid species and its hybrid ancestor

Mario Vallejo-Marin, Arielle Cooley, Michelle Qi, Madison Folmer, Michael McKain, Joshua Puzey