Biology subjects

Brevet, M.

Publications and source records attributed to Brevet, M..

5 recordsLinked to original sources

bioRxiv2024

Influence of environmental variables, small-scale fisheries and vessel traffic on the distribution and behavior of bottlenose dolphins in a tropical lagoon.

The distribution of marine predators is influenced by a variety of natural and, in some cases, anthropogenic environmental factors. In particular, the optimal foraging theory predicts that micro-habitat selection should be the result of a trade-off between prey availability, energy expenditure, and predation risk. In addition, the risk-disturbance hypothesis suggests that anthropogenic disturbance may be perceived by animals in the same way as predation risk. Habitat selection may also be locally influenced by individual behavior and physiological state (defining functional habitats): variation in their needs should affect their optimal trade-off. We tested these hypotheses in a population of bottlenose dolphins living in a tropical lagoon using a habitat modeling approach. Bottlenose dolphins were predominantly distributed within the lagoon, with a preference for the vicinity of fringing and inner reefs (with lower predation risk than the outer reef), and were located in areas of high fish productivity, consistent with optimal habitat selection. We also observed an interaction between habitat and dolphin behavior, suggesting the existence of functional habitats: foraging was more common in nearshore habitats with probable higher prey density while resting and socializing were more common further from shore. Similarly, females with calves were preferentially found in shallower waters compared to other social groups. We did not observe any effects of anthro-pogenic disturbance variables and therefore cannot conclude on the risk-disturbance hypothesis for this population.

ecology↗

bioRxiv2021

Social information use for spatial decision in Zootoca vivipara

Movements of individuals are conditioned by information acquisition coming from either personal or social sources. Yet, little is known about the processes used by individuals to make movement decisions when facing multiple sources of social information simultaneously. This study aimed to test experimentally how social information from multiple sources is used to make movement decisions, and whether a contrast in this information allows individuals to orientate in space. We used common lizards (Zootoca vivipara) in a replicated experimental setting: one focal individual received information from two other individuals coming from peripheral environments, before being given the opportunity to relocate in one or another of the peripheral environments. Our analyses revealed that the behavior of informants, their mothers morphology, as well as the quality of informants environment, affected movement decisions: the probability to relocate from the focal area increased when informants displayed traits associated with low resources (no food intake, poor maternal condition) or high competition (high activity). The physical condition of individuals also mediated the use of social information about food intake, with a match between resource availability in informants and personal condition. Conversely, spatial orientation was not affected by the contrast of phenotype between informants nor by spatial variability in resource availability. This study highlights that multiple social information sources can be used for movement decisions, likely because these information sources reflect the quality of the surrounding environment (e.g., competition level or resources availability). It also emphasizes that social information use for movement is conditioned by individual phenotype.

ecology↗

bioRxiv2021

Disentangling heterogeneity of Malignant Pleural Mesothelioma through deep integrative omics analyses

Malignant Pleural Mesothelioma (MPM) is an aggressive cancer with rising incidence and challenging clinical management. Using the largest series of whole-genome sequencing data integrated with transcriptomic and epigenomic data using multi-omic factor analysis, we demonstrate that MPM heterogeneity arises from four sources of variation: tumor cell morphology, ploidy, adaptive immune response, and CpG island methylator phenotype. Previous genomic studies focused on describing only the tumor cell morphology factor, although we robustly find the three other sources in all publicly available cohorts. We prove how these sources of variation explain the biological functions performed by the cancer cells, and how genomic events shape MPM molecular profiles. We show how these new sources of variation help understand the heterogeneity of the clinical behavior of MPM and drug responses measured in cell lines. These findings unearth the interplay between MPM functional biology and its genomic history, and ultimately, inform classification, prognostication and treatment. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/461908v1_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@b6c43corg.highwire.dtl.DTLVardef@10d45a9org.highwire.dtl.DTLVardef@58746eorg.highwire.dtl.DTLVardef@143f880_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

bioRxiv2020

The comprehensive roadmaps of reprogramming and transformation unveiled antagonistic roles for bHLH transcription factors in the control of cellular plasticity

Coordinated changes of cellular identity and plasticity are critical for pluripotent reprogramming (PR) and malignant transformation (MT). However, the molecular circuitries orchestrating these modifications, as well as their degree of analogy during reprogramming and transformation, remain unknown. To address this question, we generated "repro-transformable" mice models and dissected comparatively the early events underpinning PR - mediated by Oct4, Sox2, Klf4, c-Myc - and MT - triggered by oncogenic Ras and c-Myc. Transcriptomic analyses allowed the identification of a unique set of markers - the cell surface glycoprotein Thy1 and the transcription factor (TF) Bcl11b - that are commonly downregulated during PR and MT and delineate cellular intermediates (CI) highly amenable to generate pluripotent or malignant derivatives. Comprehensive transcriptomic, epigenomic and functional analyses of different CI, prone or refractory to PR/MT, unveiled that cellular plasticity acquisition precedes the broad extinction of cellular identity. It also demonstrated the existence of specific and shared molecular features of PR and MT while ensuring the identification of broad-range regulators of cellular plasticity. As a proof-of-concept, we revealed that the basic helix-loop-helix (bHLH) class A TF Atoh8 constrains rodent and human iPS cells generation as well as MT and direct neuron conversion. Mechanistically, this TF hampers the reactivation of the pluripotent network during PR and limits the acquisition of phenotypic plasticity during MT. Furthermore, an integrated analysis of Atoh8 genome-wide binding, alongside the other bHLH TFs c-Myc, Ascl1 and MyoD promoting reprogramming/transdifferentiation, unveiled how Atoh8 constrains cellular plasticity by occupying a specific subset of MEF enhancers and by finetuning WNT signalling activity. Collectively, by deconvoluting the early steps of the reprogramming and transformation roadmaps, this integrated study uncoupled changes of cellular plasticity and identity to shed light on novel insights into reprogramming and cancer biology. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=161 SRC="FIGDIR/small/424606v1_ufig1.gif" ALT="Figure 1"> View larger version (35K): org.highwire.dtl.DTLVardef@1718383org.highwire.dtl.DTLVardef@1714ab8org.highwire.dtl.DTLVardef@e0958borg.highwire.dtl.DTLVardef@7a0643_HPS_FORMAT_FIGEXP M_FIG C_FIG One-sentence summaryComparative roadmaps of cellular plasticity acquisition during pluripotent reprogramming and malignant transformation.

cell biology↗

bioRxiv2019

Reconstructing the history of variation in effective population size along phylogenies.

AO_SCPLOWBSTRACTC_SCPLOWThe nearly-neutral theory predicts specific relations between effective population size (Ne) and patterns of divergence and polymorphism, which depend on the shape of the distribution of fitness effects (DFE) of new mutations. However, testing these relations is not straightforward, owing to the difficulty in estimating Ne. Here, we introduce an integrative framework allowing for an explicit reconstruction of the phylogenetic history of Ne, thus leading to a quantitative test of the nearly-neutral theory and an estimation of the allometric scaling of the ratios of non-synonymous over synonymous polymorphism ({pi}N /{pi}S) and divergence (dN/dS) with respect to Ne. As an illustration, we applied our method to primates, for which the nearly-neutral predictions were mostly verified. Under a purely nearly-neutral model with a constant DFE across species, we find that the variation in{pi} N /{pi}S and dN/dS as a function of Ne is too large to be compatible with current estimates of the DFE based on site frequency spectra. The reconstructed history of Ne shows a ten-fold variation across primates. The mutation rate per generation u, also reconstructed over the tree by the method, varies over a three-fold range and is negatively correlated with Ne. As a result of these opposing trends for Ne and u, variation in{pi} S is intermediate, primarily driven by Ne but substantially influenced by u. Altogether, our integrative framework provides a quantitative assessment of the role of Ne and u in modulating patterns of genetic variation, while giving a synthetic picture of their history over the clade. SO_SCPLOWIGNIFICANCEC_SCPLOWO_SCPCAP C_SCPCAPO_SCPLOWSTATEMENTC_SCPLOWNatural selection tends to increase the frequency of mutants of higher fitness and to eliminate less fit genetic variants. However, chance events over the life of the individuals in the population are susceptible to introduce deviations from these trends, which are expected to have a stronger impact in smaller populations. In the long-term, these fluctuations, called random drift, can lead to the accumulation of mildly deleterious mutations in the genomes of living species, and for that reason, the effective population size (usually denoted Ne, and which captures the relative strength of drift, relative to selection) has been proposed as a major determinant of the evolution of genome architecture and content. A proper quantitative test of this hypothesis, however, is hampered by the fact that Ne is difficult to estimate in practice. Here, we propose a Bayesian integrative approach for reconstructing the broad-scale variation in Ne across an entire phylogeny, which in turns allows for quantifying how Ne correlates with life history traits and with various measures of genetic diversity and selection strength, between and within species. We apply this approach to the phylogeny of primates, and observe that selection is indeed less efficient in primates characterized by smaller effective population sizes.

evolutionary biology↗