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Mitochondrial function licenses oocyte fate via TORC1 activation in Drosophila [CUT&Run]

ABSTRACT: Mitochondrial dysfunction is associated with infertility and primary ovarian insufficiency (POI), yet if and how mitochondrial activity influences oocyte formation has remained unclear. We identify a metabolic check point that links mitochondrial function to oocyte fate. When mitochondrial activity is disrupted, germ cells fail to develop into oocytes. Mitochondria sustain intracellular leucine levels that activate the nutrient-sensing kinase Target of Rapamycin Complex 1 (TORC1), enabling translation of chromatin regulators that silence germ-cell programs and establish oocyte identity. Loss of mitochondrial function depletes leucine, suppresses TORC1 signaling, and arrests oocyte differentiation, whereas removal of the leucine sensor Sestrin restores both TORC1 activity and oocyte development. This metabolic check point ensures that only germ cells with functional mitochondria contribute to the maternal lineage, preserving reproductive fidelity.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE313290 | GEO | 2026/03/11

REPOSITORIES: GEO

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Mitochondrial function licenses oocyte fate via TORC1 activation in Drosophila [RNA-Seq]

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