Biology subjects

Galmiche, M.

Publications and source records attributed to Galmiche, M..

3 recordsLinked to original sources

bioRxiv2026

Supporting-like cells constitute an alternative steroidogenic lineage conserved in amniotes

In mammals, the production of sex hormones is widely considered to depend on the interstitial lineage of the gonad, which differentiates into Leydig cells in males or theca cells in females. However, certain mammalian species evidence gonadal steroidogenic activity prior to the specialization of these interstitial lineages, suggesting that alternative cell types may assume this function. Here we reveal a previously unrecognized role for supporting-like cells (SLCs), which can act as a major steroidogenic lineage during mammalian embryonic development. Through comparative single-cell transcriptomics, steroidomics and in toto organ imaging we find that in rabbits, SLCs not only contribute to the formation of gonadal rete structures, as described for other mammals, but also differentiate into a steroid-producing population. The steroidogenic program of SLCs is initially activated in both sexes but selectively maintained in ovaries, whereas in testes it is progressively replaced by that of interstitially derived Leydig cells. Evolutionary comparisons indicate that SLCs may represent an ancestral lineage that is homologous to the steroidogenic cells of non-mammalian species, which also derive from supporting precursors and share expression of cell fate regulators such as PAX2/8 and TBX1. Altogether, our findings redefine current models of gonadal lineages, revealing an unexpected plasticity in sex differentiation and exemplifying how distinct cell types can converge on analogous functions during evolution.

developmental biology↗

bioRxiv2025

Characterisation of changes in the gut microbiota associated with eating disorders

BackgroundEating disorders are serious pathologies that often begin in adolescence or young adulthood and persist for a significant period of time, with a strong negative impact on patients quality of life and mortality. The etiological origins of eating disorders are complex and involve both biological, psychological and societal factors. The gut microbiota was recently proposed as one of the potential factors involved in eating disorders. To gain a better understanding of the potential role of the gut microbiota in these diseases, we used 16S rRNA sequencing to compare the composition of the faecal microbiota of patients with all typical forms of eating disorders, i.e. anorexia nervosa, bulimia nervosa or binge-eating disorder, with that of healthy individuals. ResultsOur results demonstrate that each type of eating disorder is associated with a specific gut bacterial signature. We observed, for example, a decrease in the relative abundances of Agathobacter and Romboutsia genera and an increase in Pseudomonas in patients with anorexia, while patients with binge-eating disorder exhibit a decrease in the relative abundances of Akkermansia and Intestinimonas and an increase in Streptococcus, Eggerthella and Proteus. We also highlight a heterogeneity of gut microbiota composition in different subcategories of eating disorders, such as restricting versus binge-purge type anorexia or typical versus atypical binge-eating disorder. By focusing on the comorbidities reported by patients, we finally identified several bacterial taxa, such as Acidaminococcus and Eggerthella, whose level correlates with the occurrence of anxiety or depressive-like symptoms. ConclusionsTogether, our work demonstrates that eating disorders are associated with specific changes in gut microbiota composition and highlight the necessity to finely stratify patients to identify robust microbial signatures. In addition, we identified bacterial taxa correlating with comorbidities and decreased quality of life reported by patients. Our results now pave the way for determining the predictive value of the abundance of these taxa on the duration of the pathology or on the likelihood of relapse. They also constitute a valuable resource to further demonstrate the causal role of the gut microbiota in the onset or chronicisation of eating disorders.

microbiology↗

bioRxiv2025

Neurotoxicity of Propylene Glycol Butyl Ether: Multiomic Evidence from Human BrainSpheres

Exposure to solvents may contribute to the development of neurodevelopmental and neurodegenerative diseases. Glycol ethers consist in a widely used class of organic solvents leading to workers and consumers exposure via many different applications. Ethylene glycol ethers are gradually being replaced by propylene glycol ethers thought to be less toxic. However, their neurotoxicity is not systematically assessed prior to placing them on the market. Therefore, this study investigated the potential neurotoxicity of propylene glycol butyl ether (PGBE) for which no official occupational limit has been established. To this aim, new approach methodologies have been used. Human induced pluripotent stem cells-derived BrainSpheres model was exposed to PGBE and to its main metabolite, 2-butoxypropanoic acid (2BPA). An integrative multiomic approach (transcriptomics, proteomics, metabolomics and lipidomics) was adopted to assess molecular alterations, derive benchmark concentrations and define potential mechanisms of action. PGBE was neurotoxic at occupationally relevant exposure concentrations. This was shown for the first time in human cells. And, although PGBE was more cytotoxic than 2BPA, both compounds showed very similar neurotoxicity. PGBE and 2BPA strongly affected the cell cycle, induced oxidative stress and perturbed energy and lipid metabolism. They also targeted specific nervous system processes, such as axon guidance and synapse organization. Finally, 2BPA may trigger ferroptosis by increased iron uptake. Our results show an urgent need for public health authorities to carefully assess the risk glycol ethers pose to humans, to properly protect the workers as well as individuals in the general population unknowingly exposed from indoor air contaminations.

pharmacology and toxicology↗