Natural commensal microbes induce internal hatching in <i>C. elegans</i>.

The microbiome is increasingly recognized as a key factor of the plasticity of host life-history traits. Using the <i>Caenorhabditis elegans</i> model system, we examined how naturally associated bacterial strains affect internal egg hatching, a stress-adaptive reproductive strategy in this species. Among the bacterial strains tested, four strains (<i>Ochrobactrum</i> BH3, <i>Lelliottia</i> JUb66, <i>Pantoea</i> BIGb0393, and <i>Enterobacter</i> CEent1) induced high levels of internal hatching (28-57%) in <i>C. elegans</i> during late adulthood, compared to <5% in animals grown on <i>E. coli</i> OP50. These effects were accompanied by extending the reproductive window while showing a trend toward reduced total progeny and lifespan. Genetic analyses revealed that these effects are mediated through various components of the insulin signaling pathway: the <i>α-proteobacterial</i> strain BH3 acts via DAF-16/FOXO, whereas the three γ<i>-proteobacterial</i> strains act independently of DAF-16, suggesting differences in pathway dependence. Our findings demonstrate that naturally associated microbiome members can differentially interact with host endocrine signaling to shape reproductive outcomes. These results underscore the role of microbial cues in shaping life-history plasticity in animals.IMPORTANCEMicrobiome members profoundly influence host physiology, including reproductive strategies. Using the <i>Caenorhabditis elegans</i> natural microbiome model, we show that commensal bacteria can induce internal egg hatching, a facultative vivipary phenotype previously linked primarily to early-life starvation or pathogen exposure that severely reduces reproductive output. In contrast, commensal strains trigger this shift mainly in late adulthood, extending the reproductive window with minimal impact on overall fecundity. We further demonstrate that bacterial strains act through distinct components of the host insulin signaling pathway. More broadly, these findings highlight diverse avenues within conserved endocrine networks that are susceptible to microbial modulation and underscore the potential to leverage microbiomes to influence host life-history traits.