Mitofusin 1 is required for the oocyte-granulosa cell communication that regulates oogenesis
Mitochondrial function, largely regulated by the dynamics of this organelle, is inextricably linked to oocyte health. While the proteins that modulate mitochondrial fusion, Mitofusin 1 (MFN1) and 2 (MFN2), are required for embryogenesis, their role in oocyte development remains unclear. Here we show that the oocyte-specific deletion of Mfn1, but not Mfn2, results in a complete loss of oocyte growth and ovulation due to a block in folliculogenesis at the preantral-to-antral follicle transition. We pinpoint the loss of oocyte ovulation to disrupted oocyte-somatic cell communication - Mfn1-null oocytes are deficient for the production of the important somatic cell signaling factor GDF9. Unexpectedly, the double loss of Mfn1 and Mfn2 mitigates the effects on oocyte growth and ovulation, which is explained by a partial rescue of oocyte-somatic cell communication and folliculogenesis. Together, this work demonstrates that mitochondrial function influences communication of oocyte with follicular somatic cells and suggests that the balanced expression of modulators of mitochondrial dynamics is critical for proper oocyte development.