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. Surprisingly, however, functions in the tyramine/octopaminergic neurons (OPNs) and not in the ovaries or the insulin-producing cells (IPCs). Consistently, knockdown of in only the OPNs is sufficient to mimic the ovarian phenotype, while expression of the gene in the OPNs alone can 'rescue' the mutant defect. Last, we have identified and as critical targets of This study thus identifies as a novel molecular player in the brain-gonad axis and underscores the significance of inter-organ systemic communication during development.