Mon1 constitutes a novel node in the brain-gonad axis that is essential for female germline maturation.

Monensin-sensitive 1 (Mon1) is an endocytic regulator that participates in the conversion of Rab5-positive early endosomes to Rab7-positive late endosomes. In , loss of leads to sterility as the mutant females have extremely small ovaries with complete absence of late stage egg chambers - a phenotype reminiscent of mutations in the insulin pathway genes. Here, we show that expression of many insulin-like peptides (ILPs) is reduced in mutants and feeding adults an insulin-rich diet can rescue the ovarian defects.