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

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.