Polycomb Group Proteins Are Required For The Development Of Drosophilaoptic Lobe

The Polycomb group (PcG)proteins are first found in Drosophila embryo, where theyare required for establishing a repressive state of Hox gene expression. Recently, it hadbeen shownthat PcG proteins could take part in almost all the important developmentalstages, such as development of embryonic stem cell and adult stem cell, and tumorgenesis. However, the mechanism of its function in the nervous system is not very clear.In this study, we have examined the requirement of PcG proteinsduring thedevelopment of Drosophila brain. We examineseveral components of PcG proteins,including Ph,Psc-Su(z)2, Pc, E(z), et al., andfind that loss of PcG function causesinstability of neuroepithelial (NE) cells in the optic lobe and inhibits NE cellsproliferation and their differentiation into neuroblasts. Hox genes abdA and Abd-B areup-regulated in PcG mutant cells, while ectopic expression of Hox genes mimics loss ofPcG function. Loss of Ph or Pc leads to JAK/STAT pathway activation but Notchpathway inactivation; a decrease of STAT92E activity in ph mutant cells partiallyrescues the differentiation of NE cells to neuroblasts. Meanwhile some segmentationgenes are ectopically expressed in the mutant neurons, which means the type of theneurons may have changed.Our study thus suggests that PcG proteins are required for the stability andproliferation of the NE cells, and promotes their ability of differentiation into theprogenitor cells, maybe through Hox gene and JAK/STAT pathway. PcG proteins canalso regulate the types of the neurons in the optic lobe.Treh gene encodes trehalase, which is one of the most important hydrolases ininsects, and provides the source of energy by hydrolyze the trehalose into glucose. Butfew work focused on its function during developmental progress. In this study, we findloss ofTrehgene causes disintegration of NE cells and premature differentiation intoneuroblasts in the Drosophila optic lobe. Thus, we conclude that Treh gene can maintainthe NE cells and inhibit their differentiation into neuroblasts, however independent oftrehalose metabolism.