# Somatic Kitl promotes mTOR to facilitate prophase I of meiosis in female embryonic gonads

## TL;DR

This study reveals that Kitl signaling from somatic cells promotes meiosis in female mouse embryos by activating mTOR pathways.

## Contribution

The study identifies Kitl/Kit signaling as a novel regulator of meiotic prophase I in fetal germ cells.

## Key findings

- Disruption of Kitl/Kit signaling impairs meiosis initiation and homologous synapsis.
- Kitl/Kit activates mTOR/p-S6 signaling to elevate proteins like Stra8, Sycp1, and Sycp3.
- mTOR activation rescues meiotic defects caused by Kitl deficiency.

## Abstract

Homologous synapsis and recombination are the central events that take place in the prophase I of meiosis. Signaling that promotes the germ cell differentiation and prophase I remains elusive. Here we show a key Kitl/Kit signaling between somatic cells and germ cells in regulating meiotic prophase I in the mouse fetal gonad. Disruption of Kitl/Kit signaling, both in vivo and in vitro, impairs meiosis initiation, disrupts homologous synapsis and recombination. Moreover, mTOR/p-S6 signaling induced by Kitl/Kit elevates the levels of critical proteins such as Stra8, Sycp1 and Sycp3 for meiosis entry and homologous synapsis. Blocking Kitl/Kit signaling suppresses the mTOR and decreases the protein levels of Stra8, Sycp1, Sycp3 and Vasa, impairing the prophase I. In contrast, activating mTOR can rescue the meiotic defects caused by somatic Kitl deficiency. The activated p-AKT links Kitl/Kit to promoting mTOR/p-S6 signaling in the fetal germ cells. These findings reveal the critical functions and mechanisms of somatic Kitl in meiosis entry and homologous synapsis and recombination during the prophase I.