Abstract
We investigated the role of oxygen-sensing atypical guanylyl cyclase subunit Gyc89Db in the developing brain. Despite its expression in the hypoxic neuroepithelium of the larval optic lobe of Drosophila , loss-of-function mutants and ectopic expression did not alter neuroepithelial cell number or proliferation. Notably, while ectopic expression of Gyc89Db increases optic lobe volume and neuroblast numbers, our negative results suggest that these effects manifest earlier in development without persistent alteration of the neuroepithelium, through mechanisms that might be independent of neuroepithelial proliferation.