ENS - MemoLife

Odile MALIET

Godfroid — 2020-12-22T08:31:49Z

Abstract

How ecological interaction networks emerge on evolutionary time scales remains unclear. Here we build an individual‐based eco‐evolutionary model for the emergence of mutualistic, antagonistic and neutral bipartite interaction networks. Exploring networks evolved under these scenarios, we find three main results. First, antagonistic interactions tend to foster species and trait diversity, while mutualistic interactions reduce diversity. Second, antagonistic interactors evolve higher specialisation, which results in networks that are often more modular than neutral ones ; resource species in these networks often display phylogenetic conservatism in interaction partners. Third, mutualistic interactions lead to networks that are more nested than neutral ones, with low phylogenetic conservatism in interaction partners. These results tend to match overall empirical trends, demonstrating that structures of empirical networks that have most often been explained by ecological processes can result from an evolutionary emergence. Our model contributes to the ongoing effort of better integrating ecological interactions and macroevolution.

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Ecol Lett. 2020 Sep 4. doi : 10.1111/ele.13592

Hélène Morlon | IBENSAmaury Lambert | CIRB

Godfroid — 2020-09-08T10:52:47Z

Abstract

In standard models of molecular evolution, DNA sequences evolve through asynchronous substitutions according to Poisson processes with a constant rate (called the molecular clock) or a rate that can vary (relaxed clock). However, DNA sequences can also undergo episodes of fast divergence that will appear as synchronous substitutions affecting several sites simultaneously at the macroevolutionary time scale. Here, we develop a model, that we call the Relaxed Clock with Spikes model (RCS), combining basal, clock-like molecular substitutions with episodes of fast divergence called spikes arising at speciation events. Given a multiple sequence alignment and its time-calibrated species phylogeny, our model is able to detect speciation events (including hidden ones) co-occurring with spike events and to estimate the probability and amplitude of these spikes on the phylogeny. We identify the conditions under which spikes can be distinguished from the natural variance of the clock-like component of molecular substitutions and from variations of the clock. We apply the method to genes underlying snake venom proteins and identify several spikes at gene-specific locations in the phylogeny. This work should pave the way for analyses relying on whole genomes to inform on modes of species diversification.

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Mol Biol Evol. 2020 Jun 10 ; msaa144. doi : 10.1093/molbev/msaa144.

Virginia Busetto,

Godfroid — 2020-07-21T14:22:12Z

V. Busetto, I. Barbosa, J. Basquin, E. Marquenet, R. Hocq, M. Hennion, J.A. Paternina, A. Namane, E. Conti, O. Bensaude, H. Le Hir

Abstract

Human CWC27 is an uncharacterized splicing factor and mutations in its gene are linked to retinal degeneration and other developmental defects. We identify the splicing factor CWC22 as the major CWC27 partner. Both CWC27 and CWC22 are present in published Bact spliceosome structures, but no interacting domains are visible. Here, the structure of a CWC27/CWC22 heterodimer bound to the exon junction complex (EJC) core component eIF4A3 is solved at 3Å-resolution. According to spliceosomal structures, the EJC is recruited in the C complex, once CWC27 has left. Our 3D structure of the eIF4A3/CWC22/CWC27 complex is compatible with the Bact spliceosome structure but not with that of the C complex, where a CWC27 loop would clash with the EJC core subunit Y14. A CWC27/CWC22 building block might thus form an intermediate landing platform for eIF4A3 onto the Bact complex prior to its conversion into C complex. Knock-down of either CWC27 or CWC22 in immortalized retinal pigment epithelial cells affects numerous common genes, indicating that these proteins cooperate, targeting the same pathways. As the most up-regulated genes encode factors involved in inflammation, our findings suggest a possible link to the retinal degeneration associated with CWC27 deficiencies.

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Nucleic Acids Res. 2020 Jun 4 ;48(10):5670-5683. doi : 10.1093/nar/gkaa267

Isma Bennabi

Godfroid — 2020-04-07T15:01:30Z

Isma Bennabi, Flora Crozet°, Elvira Nikalayevich°, Agathe Chaigne, Gaëlle Letort, Marion Manil-Ségalen, Clément Campillo, Clotilde Cadart, Alice Othmani, Rafaele Attia, Auguste Genovesio, Marie-Hélène Verlhac* & Marie-Emilie Terret*.
(°equal contribution, *co-corresponding authors)

Abstract

Human and mouse oocytes' developmental potential can be predicted by their mechanical properties. Their development into blastocysts requires a specific stiffness window. In this study, we combine live-cell and computational imaging, laser ablation, and biophysical measurements to investigate how deregulation of cortex tension in the oocyte contributes to early developmental failure. We focus on extra-soft cells, the most common defect in a natural population. Using two independent tools to artificially decrease cortical tension, we show that chromosome alignment is impaired in extra-soft mouse oocytes, despite normal spindle morphogenesis and dynamics, inducing aneuploidy. The main cause is a cytoplasmic increase in myosin-II activity that could sterically hinder chromosome capture. We describe here an original mode of generation of aneuploidies that could be very common in oocytes and could contribute to the high aneuploidy rate observed during female meiosis, a leading cause of infertility and congenital disorders.

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Nat Commun. 2020 Apr 3 ;11(1):1649. doi : 10.1038/s41467-020-15470-y.