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0This scientific article demonstrates that Kitl/Kit signaling between somatic granulosa cells and germ cells is essential for the initiation and progression of meiosis in female mouse embryos. By utilizing conditional knockout models and single-cell RNA sequencing, the researchers found that a lack of Kitl leads to significant defects in homologous synapsis, DNA repair, and crossover formation during prophase I. The study reveals that this regulation occurs through the activation of the mTOR pathway, which is driven by p-AKT signaling within the fetal germ cells. Experimental results show that inhibiting either Kit or mTOR suppresses meiotic entry, while activating mTOR can rescue the developmental failures caused by Kitl deficiency. These findings suggest that the Kitl-Kit-mTOR axis acts as a critical regulatory mechanism that functions largely independently of retinoic acid to control germ cell differentiation. Ultimately, the research identifies a vital communication link between the gonadal environment and the genetic events necessary for producing viable oocytes.
References:
Liu C, Jin Z, Chen J, et al. Somatic Kitl promotes mTOR to facilitate prophase I of meiosis in female embryonic gonads[J]. Cell Death & Disease, 2025, 16(1): 838.
