Kitl/kit signaling pathway regulate meiosis in mouse female gonad

The initiation of meiotic division, proper homologous chromosome pairing, and recombination are essential for maintaining genome stability in gametes. Numerous genes are involved in regulating these key processes during meiosis. However, the role of gonad somatic cells in regulating the initiation and progression of germ cell meiosis remains poorly understood. In this study, we identify the Kitl/Kit signaling pathway as a critical regulator of meiotic in female gonads. Disruption of Kitl/Kit signaling, both in vivo and in vitro, impairs the initiation of meiosis and leads to abnormalities in meiotic progression. We also observed that the mTOR/S6 signaling pathway is inhibited when Kitl/Kit signaling is blocked. Notably, adding a mTOR activator to in vitro cultures of Kitl conditional knockout gonads partially rescued germ cell numbers and improved meiotic initiation efficiency. Our findings highlight the essential role of the Kitl-Kit-mTOR-S6 signaling axis in meiotic initiation and progression. This study reveals a novel function of Kitl/Kit signaling in regulating embryonic meiosis and provides a new framework for future research on how somatic cells influence germ cell meiosis. Primary satellite cells were isolated from C57BL/6 mice. Cells were cultured in growth medium and treated with either rhMG53 protein or BSA (as vehicle control) for 3 days. Total RNA was harvested from 3 biological replicates per group (Total N=6). Comparative gene expression analysis was performed to identify differentially expressed genes (DEGs) between MG53-treated and Control groups.