Biology subjects

Loison, L.

Publications and source records attributed to Loison, L..

4 recordsLinked to original sources

bioRxiv2025

The Baldwin effect reloaded: Intermediate levels of phenotypic plasticity favor evolutionary rescue

Since the late 1890s and until today, how phenotypic plasticity interacts with genetic adaptation is a debated issue. Proponents of a positive causal role of phenotypic plasticity -James M. Bald-win in the first place- supported the view that, in altered environmental conditions, phenotypic plasticity is a key factor allowing a population to avoid extinction and then genetic evolution to catch up ("Original Baldwin Effect", thereafter OBE). Opponents, like for instance Ernst Mayr, regularly pointed out that phenotypic plasticity, by masking genetic variation, slows gene-level evolution ("Mayr Effect", thereafter ME). For decades this opposition remained only verbal and qualitative. To resolve it, we propose here a stochastic model that, following Baldwins intuitive take, combines the minimal number of ingredients to account for extinction, selection, mutation and plasticity. We study evolutionary rescue of the population (arrival and invasion of an adaptive genetic mutant) in the altered environment for different values of phenotypic plasticity, here quantified as the probability p that the maladapted genotype develops into the adapted phenotype. Our claim is that OBE can be a genuine evolutionary mechanism, depending on the level of phenotypic plasticity with respect to a threshold value p[*]: when p < p[*], increasing p promotes evolutionary rescue by delaying extinction ("Strong" OBE); when p > p[*], plasticity sustains population survival and increasing p has two antagonistic effects: to accelerate adaptation by increasing the supply of adaptive mutants ("Weak" OBE, intermediate values of p), and to slow down adaptation by decreasing their fitness advantage (ME, high values of p).

evolutionary biology↗

bioRxiv2024

Gut microbiota regulates food intake in a rodent model of binge-eating disorder

ObjectiveBinge-eating disorder is characterized by recurrent episodes of consumption of large amounts of food within a short period of time, without compensatory behaviours. This disease is a major public health issue since it decreases patients quality of life and is associated with numerous comorbidities, encompassing anxiety, depression and complications associated with obesity. The pathophysiology of binge-eating disorder is complex and involves both endogenous, environmental and sociocultural factors. The gut microbiota has been proposed to be an important player in the onset or maintenance of eating disorders. Here, we aim to better delineate the potential role of the gut microbiota in binge-eating disorder. MethodWe used a model of binge-eating disorder where eight-weeks-old C57Bl/6 female mice had access during 2 hours, every 2 days over a 10-day period, to a highly palatable and high-calorie diet. Half of the animals received antibiotics to deplete their gut microbiota. Eating behaviour and other behavioural parameters were compared between groups. ResultsWe observed an increase in food intake in mouse exposed to high-fat high-sucrose diet, as well as tachyphagia and craving for food during binge-eating episodes. We demonstrate the gut microbiota depletion further increases food intake, specifically during binge-eating episodes. DiscussionThese results show that the gut microbiota is involved in the control of food intake during episodes of binge-eating. This strengthens the potential role of the gut bacteria in binge-eating disorder and open the way for future therapeutic strategies aiming at targeting patients gut microbiota.

animal behavior and cognition↗

bioRxiv2024

Staphylococcus warneri dampens SUMOylation and promotes intestinal inflammation

Gut bacteria play key roles in intestinal physiology, via the secretion of diversified bacterial effectors. Many of these effectors remodel the host proteome, either by altering transcription or by regulating protein post-translational modifications. SUMOylation, a ubiquitin-like post-translational modification playing key roles in intestinal physiology, is a target of gut bacteria. Mutualistic gut bacteria can promote SUMOylation, via the production of short- or branched-chain fatty acids (SCFA/BCFA). In contrast, several pathogenic bacteria were shown to dampen SUMOylation in order to promote infection. Here, we challenge this dichotomic vision by showing that Staphylococcus warneri, a non-pathogenic bacterium of the human gut microbiota, decreases SUMOylation in intestinal cells. We identified that Warnericin RK, a hemolytic toxin secreted by S. warneri, targets key components of the host SUMOylation machinery, leading to the loss of SUMO-conjugated proteins. We further demonstrate that the dampening of SUMOylation triggered by Warnericin RK promotes inflammation, and, more particularly, TNF-dependent intestinal inflammatory responses. Together, these results highlight the diversity of mechanisms used by non-pathogenic bacteria from the gut microbiota to manipulate host SUMOylation. They further highlight that changes in gut microbiota composition may impact intestinal inflammation, by changing the equilibrium between bacterial effectors promoting or dampening SUMOylation.

microbiology↗

bioRxiv2022

Fatty acids produced by the gut microbiota dampen host inflammatory responses by modulating intestinal SUMOylation

The gut microbiota produces a wide variety of metabolites, which interact with intestinal cells and contribute to host physiology. These metabolites regulate intestinal cell activities by modulating either gene transcription or post-translational modifications of gut proteins. The effect of gut commensal bacteria on SUMOylation, an essential ubiquitin-like modification in intestinal physiology, remains however unknown. Here, we show that short chain fatty acids (SCFAs) and branched chain fatty acids (BCFAs) produced by the gut microbiota increase protein SUMOylation in different intestinal cell lines in a pH-dependent manner. We demonstrate that these metabolites induce an oxidative stress which inactivates intestinal deSUMOylases and promotes the hyperSUMOylation of chromatin-bound proteins. In order to determine the impact of these modifications on intestinal physiology, we focused on the NF-{kappa}B signaling pathway, a key player in inflammation known to be regulated by SUMOylation. We demonstrated that the hyperSUMOylation induced by SCFAs/BCFAs inhibits the activation of the NF-{kappa}B pathway in intestinal cells by blocking the degradation of the inhibitory factor I{kappa}B in response to TNF. This results in a decrease in pro-inflammatory cytokines expression, such as IL8 or CCL20, as well as a decrease in intestinal epithelial permeability in response to TNF. Together, our results reveal that fatty acids produced by gut commensal bacteria regulate intestinal physiology by modulating SUMOylation and illustrate a new mechanism of dampening of host inflammatory responses by the gut microbiota.

cell biology↗