Biology subjects

Roux, P.

Publications and source records attributed to Roux, P..

7 recordsLinked to original sources

bioRxiv2026

Quantitative evaluation of enrichment protocols on rhesus macaques welfare in laboratory environment.

Non-human primates are crucial animal models in biomedical research including neurosciences. Legal frameworks ensure that participation of monkeys in biomedical research follows an ethical assessment, driven by specific guidelines for ensuring animal well-being. Those guidelines promote continued refinement of practices to improve animal wellbeing, yet quantitative data to inform such refinements is limited. In this context, we investigated the impact of modifications to the housing that created either navigational complexity or visual access to neighbouring animals on the behaviour of rhesus macaques. Then we quantified the value of different enrichment programmes based on manipulable objects. We showed that making navigation within a modular housing more complex, or adding transparent separations between housing units is associated with significant reduction of severe aggression, stereotypical behaviours and a significant increase of appeasing behaviours. We also observed a positive effect of manipulable objects with an increase in the expression of appeasing behaviours and a decrease in abnormal or stereotypical behaviours. Finally, our study revealed significant inter-individual variability that was not explained by sex, age, social network size or social status. Overall, our results point to the importance and benefits of environmental changes and enrichment protocols, and of the critical need for personalised enrichment programmes.

animal behavior and cognition↗

bioRxiv2024

A shared genetic basis for sexually antagonistic male and female adaptations in the toothed water strider

Sexual conflict can drive the divergence of male and female phenotypes and several cross-species comparative analyses have documented patterns of correlated evolution of sex-specific traits that promote the evolutionary interests of the sexes. However, male-female coevolution can be highly dynamic. Moreover, if male and female traits do not have an entirely distinct genetic basis, this can have profound effects on their coevolutionary dynamics. Here, we use water striders, a well-studied model system for sexually antagonistic coevolution, and ask whether sex-specific phenotypic adaptations covary across populations and whether they share a common developmental genetic basis. Using comparative analyses both at the population and species levels, we document an association between a derived male mate-grasping trait and a likely female anti-grasping counteradaptation in the toothed water strider Gerris odontogaster. Interestingly, in one population where males did not express their derived grasping trait, females had also regained the ancestral morphology. We then used experimental manipulation of gene expression, and show that these male and female traits are both linked to a common developmental genetic program containing Hox and sex determination genes, despite the fact that they are different structures on different segments. Our work thus suggests that the pleiotropic nature of developmental genetic programs can blur the distinction between inter- and intralocus genetic conflict.

evolutionary biology↗

bioRxiv2023

Mitochondrial Biomarkers and Metabolic Syndrome in Bipolar Disorder

ImportanceExamining translatable mitochondrial blood-based biological markers to identify its association with metabolic diseases in bipolar disorder. ObjectiveTo test whether mitochondrial metabolites, mainly lactate, and cell-free circulating mitochondrial DNA are associated with markers of metabolic syndrome in bipolar disorder, hypothesizing higher lactate but unchanged cell-free circulating mitochondrial DNA levels in bipolar disorder patients with metabolic syndrome. DesignIn a cohort study, primary testing from the FondaMental Advanced Centers of Expertise for bipolar disorder was conducted, including baseline plasma samples and blinded observers for all experimentation and analysis. SettingThe FondaMental Foundation coordinate a multicenter, multidisciplinary French networks aiming at creation of cohorts to improve identification of homogeneous subgroups of psychiatric disorders toward personalized treatments. ParticipantsThe FACE-BD primary testing cohort includes 837 stable bipolar disorder patients. The I-GIVE validation cohort consists of 235 participants: stable and acute bipolar patients, non-psychiatric controls, and acute schizophrenia patients. Participants were randomly selected based on biosample availability. ExposuresAll patients underwent the standard primary care within their center. No intentional exposures were part of this study. Main Outcome and MeasuresThe primary outcome modelled an association with lactate and metabolic syndrome in this population. Reflective a priori hypothesis. ResultsMultivariable regression analyses show lactate association with triglycerides (Est= 0.072(0.023), p = 0.0065,), fasting glucose (Est = 12(0.025), p= 0.000015) and systolic (Est= 0.003(0.0013), p= 0.031) and diastolic blood pressure (Est = 0.0095{+/-}0.0017, p= 1.3e-7). Significantly higher levels of lactate were associated with presence of metabolic syndrome (Est = 0.17{+/-}0.049, p=0.00061) after adjusting for potential confounding factors. Mitochondrial-targeted metabolomics identified distinct metabolite profiles in patients with lactate presence and metabolic syndrome, differing from those without lactate changes but with metabolic syndrome. Circulating cell-free mitochondrial DNA was not associated with metabolic syndrome. Conclusion & RelevanceThis thorough analysis mitochondrial biomarkers indicate the associations with lactate and metabolic syndrome, whereas circulating cell-free mitochondrial DNA is limited in the context of metabolic syndrome. This study is relevant to improve the identification and stratification of bipolar patients with metabolic syndrome and provide potential personalized-therapeutic opportunities. Key PointsO_ST_ABSQuestionC_ST_ABSCan lactate, a mitochondrial metabolite, indicate metabolic syndrome in bipolar disorder? FindingIn 837 stable bipolar disorder patients, we found high lactate levels significantly associated with metabolic syndrome, unlike circulating cell-free mitochondrial DNA. This pattern also appeared in acute bipolar and schizophrenia cases. Mitochondrial-targeted metabolomics distinguishes patients with high lactate and metabolic syndrome from those without lactate changes, but presence of metabolic syndrome. MeaningThis research underscores lactate as a potential biomarker for identifying bipolar disorder patients with metabolic syndrome. It opens new avenues for personalized treatment strategies, leveraging mitochondrial metabolite profiling to improve patient stratification and therapeutic outcomes.

neuroscience↗

bioRxiv2022

New insights from short and long reads sequencing to explore cytochrome b variants of Plasmopara viticola populations collected in vineyard and related to resistance to complex III inhibitors

Downy mildew is caused by Plasmopara viticola, an obligate oomycete plant pathogen, a devasting disease for grapevine. To preserve plants from the disease, complex III inhibitors are among the widely used fungicides that specifically target the mitochondrial cytochrome b (cytb) of the pathogen to block cellular respiration mechanisms. In French vineyard, P. viticola developed resistance against a first category of these fungicides, the Quinone outside inhibitors, by exhibiting a single amino acid substitution G143A in its cytb mitochondrial sequence. Their usage was restricted and another kind of fungicides, Quinone inside inhibitors, targeting the same gene and highly effective against oomycetes, were used instead. Recently however, less sensitive P. viticola populations were detected after treatments with some inhibitors, in particular ametoctradin and cyazofamid. By isolating resistant single-sporangia strains of P. viticola to these fungicides, we characterized new variants in cytb sequences associated with cyazofamid resistance: a point mutation (L201S) and more strikingly, two insertions (E203-DE-V204, E203-VE-V204). In parallel with classical tools, pyrosequencing and RT-PCR, we then benchmarked both short and long-reads NGS technologies (Ion Torrent, Illumina, Oxford Nanopore Technologies) to sequence the complete cytb with the prospect to detect and assess the proportion of resistant variants of P. viticola at a natural population scale. Eighteen populations collected from French vineyard fields in 2020 were analysed: 12 show a variable proportion of G143A, 11 of E203-DE-V204 and 7 populations of the S34L variant that confers resistance to ametoctradin. Interestingly, long reads were able to identify variants, including SNPs, with confidence and detect a small proportion of P. viticola showing several variants along the same cytb sequence. Altogether, NGS appear promising methods to evaluate pathogen resistance towards fungicides related to cytb modifications at a population scale in the field. This approach could be rapidly a robust decision-support management tool for vineyard in future.

evolutionary biology↗

bioRxiv2021

Peer presence and familiarity as key factors to reduce cocaine intake: an effect mediated by the Subthalamic Nucleus

Stimulant use, including cocaine, often occurs in a social context whose influence is important to understand to decrease intake and reduce associated harms. Given the regulatory role of the subthalamic nucleus (STN) on cocaine intake and emotions, we investigate its role on such influence of social context on cocaine intake. We explored the influence of peer presence and familiarity on the frequency of self-administered cocaine and its neurobiological basis. We first compared cocaine intake in various conditions (alone or with peers with different characteristics: observing or self-administering, familiar or not, cocaine-naive or not, dominant or subordinate) in rats (n=90). The risk of drug consumption was reduced when a peer was present, observing or self-administering as well, and further diminished when the peer was unfamiliar (vs familiar). The presence of a cocaine-naive peer further decreased cocaine consumption. The presence of a non-familiar and drug-naive peer represents thus key conditions to diminish cocaine intake. We tested the effects of STN lesions in these various conditions and also conducted social experiments to validate the role of STN in social cognition. The STN lesion by itself reduced cocaine intake to the level reached in presence of a stranger naive peer and affected social cognition, positioning the STN as one neurobiological substrate of social influence on drug intake. Finally, with a translational research approach, we compared the drug intake in these conditions in human drug users (n=77). This human study confirmed the beneficial effect of social presence, especially of strangers. Our results indirectly support the use of social interventions and harm reduction strategies, in particular supervised consumption rooms for stimulant users.

neuroscience↗

bioRxiv2021

Adaptation to DNA damage as a bet-hedging mechanism in a fluctuating environment

In response to DNA damage, efficient repair is essential for cell survival and genome integrity. In eukaryotes, the DNA damage checkpoint is a signalling pathway that coordinates this response and arrests the cell cycle to provide time for repair. However, when repair fails or when the damage is not repairable, cells can eventually bypass the DNA damage checkpoint and undergo cell division despite persistent damage, a process called adaptation to DNA damage. Interestingly, adaptation occurs with a delayed timing compared to repair and shows a large variation in time, two properties that may provide a survival advantage at the population level without interfering with repair. Here, we explore this idea by mathematically modelling cell survival in response to DNA damage and focusing on adaptation parameters. We find that the delayed adaptation timing indeed maximizes survival, but its heterogeneity is beneficial only in a fluctuating damage-inducing environment. Finally, we show that adaptation does not only contribute to survival but also to genome instability and mutations, which might represent another criterion for its selection through-out evolution. Overall, we propose that adaptation can act as a bet-hedging mechanism for cell survival in response to DNA damage.

bioinformatics↗

bioRxiv2018

Of Rats And Men: Peer Presence And Familiarity Are Key Factors Which Modulate Drug Intake

Social environment influences drug consumption, its persistence and evolution. Little is known regarding the influence of the presence of a peer during drug consumption and especially how the relationship between peers (familiarity and dominance) can influence drug consumption. We used here a translational and transdisciplinary approach to explore the influence of peer presence and peer familiarity in rats and humans that self-administer stimulants. In rats, cocaine intake was compared when rats were alone with intake when peers with different characteristics (familiar or not, cocaine naive or not, dominant or subordinate) were present. In humans, 77 cocaine and/or methylphenidate users were asked to detail their most recent drug use episodes and their relationship with peers present at consumption. The results show that in both humans and rats, the risk of cocaine/stimulant consumption was significantly reduced by 37% and 32%, respectively, when a peer was present. Moreover, the lowest risk of consumption was consistently observed when the peer was unfamiliar (vs familiar) with a further 38% and 17% risk reduction, respectively. In rats, a decreased risk of consumption was greater when the peer was cocaine naive (vs non-cocaine naive).\n\nThe presence of a non-familiar and possibly drug-naive peer is the most efficient condition to diminish stimulant intake. Our results indirectly support the use of harm reduction strategies, in particular supervised consumption rooms for stimulant users.

neuroscience↗