Exploring the role of Mon1 in Drosophila ovary development

Abstract

The involvement of the nervous system and the mechanisms regulating organ development and regeneration is a area that is gaining prominence. In the present study, we have tried to understand the molecular basis for sterility in Dmon1 mutants. These mutants show extremely small ovaries with fewer ovarioles and egg chambers that fail to progress through the vitellogenic phase. We find that neuronal expression of Dmon1 rescues the ovary phenotypes. More specifically, we find that expression in octopaminergic neurons is sufficient for the rescue. Using RNAi against Dmon1, we show that the phenotype is neuronal in origin and not ovarian suggesting that Mon1 regulates Drosophila ovary development in non-cell autonomous manner. To understand the mechanism of this regulation we have examined the role of insulin signaling in these mutants. We find that expression of some of the dilps is significantly reduced in Dmon1Δ181 mutants (mutants carrying a deletion of the C-terminus) and feeding insulin to Dmon1Δ181 flies results in the rescue of the ovary phenotypes and a mild improvement in life span. Our results suggest that Dmon1 regulates ovary development by regulating the synthesis and/or secretion of insulin-like peptides in the brain.