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SYISL affects fetal mice muscle fiber number by regulating maternal intestinal microbiota and their metabolites

ABSTRACT: The formation of embryonic muscle fibers during the prenatal period determines the number of muscle fibers after birth. Our previous studies showed that SYISL gene knockout (KO) mice significantly increased the number of total muscle fibers, but the underlying mechanism remains unclear. In this study, we found that the development of embryonic muscle fibers was significantly influenced by the interaction between host SYISL genotype and maternal gut microbiota. SYISL KO alters the composition of the female mice maternal gut microbiota, significantly increases the relative abundance of Prevotella (P<0.05). Fecal microbiota transplantation (FMT) experiments indicated that fecal suspension from KO female mice significantly increased the number of offspring muscle fibers. Our study provides the new evidence for the interaction between maternal single gene and gut microbiota on the embryonic muscle development of the offspring.

ORGANISM(S): Mus musculus

PROVIDER: GSE244822 | GEO | 2025/02/19

REPOSITORIES: GEO

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Project description:“Dysbiosis" of the maternal gut microbiome, in response to environmental challenges such as infection, altered diet and stress during pregnancy, has been increasingly associated with abnormalities in offspring brain function and behavior. However, whether the maternal gut microbiome regulates neurodevelopment in the absence of environmental challenge remains unclear. In addition, whether the maternal microbiome exerts such influences during critical periods of embryonic brain development is poorly understood. Here we investigate how depletion, and selective reconstitution, of the maternal gut microbiome influences fetal neurodevelopment in mice. Embryos from antibiotic-treated and germ-free dams exhibit widespread transcriptomic alterations in the fetal brain relative to conventionally-colonized controls, with reduced expression of several genes involved in axonogenesis. In addition, embryos from microbiome-depleted mothers exhibit deficient thalamocortical axons and impaired thalamic axon outgrowth in response to cell-extrinsic guidance cues and growth factors. Consistent with the importance of fetal thalamocortical axonogenesis for shaping neural circuits for sensory processing, restricted depletion of the maternal microbiome from pre-conception through mid-gestation yields offspring that exhibit tactile hyposensitivity in select sensorimotor behavioral tasks. Gnotobiotic colonization of antibiotic-treated dams with a limited consortium of spore-forming bacteria indigenous to the gut microbiome prevents abnormalities in fetal brain gene expression, fetal thalamocortical axonogenesis and adult tactile sensory behavior associated with maternal microbiome depletion. Metabolomic profiling reveals that the maternal microbiota regulates levels of numerous small molecules in the maternal serum as well as the brains of fetal offspring. Select microbiota-dependent metabolites – trimethylamine N-oxide, 5-aminovalerate, imidazole propionate, and hippurate – sufficiently promote axon outgrowth from fetal thalamic explants. Moreover, maternal supplementation with the metabolites during early gestation abrogates deficiencies in fetal thalamocortical axons and prevents abnormalities in tactile sensory behavior in offspring from microbiome-depleted dams. Altogether, these findings reveal that the maternal gut microbiome promotes fetal thalamocortical axonogenesis and select tactile sensory behaviors in mice, likely by signaling of microbially modulated metabolites to neurons in the developing brain.

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SYISL affects fetal mice muscle fiber number by regulating maternal intestinal microbiota and their metabolites

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