Phyllopod-Mediated Protein Degradation in Drosophila Neural Development

The development of nervous system requires coordinated regulation in cell fate specification and cell cycle control. During Drosophila external sensory (ES) organ development, the ubiquitin E3 ligase adaptor Phyllopod (Phyl) plays a critical role in specifying neural cell fate. In phyl mutants, specification of the sensory organ precursor (SOP), the primary neural progenitor in ES organ development, is severely disrupted. In addition, the timing of G2/M progression of SOP is delayed in phyl mutants. Our recent analyses suggest that phyl promotes G2/M progression of SOPs by mediating the proteolysis of bHLH proneural proteins Achaete (Ac) and Scute (Sc). In the first part of this proposal, we would like to first examine the specificity of this degradation in other neuronal lineages of Drosophila peripheral nervous system. Second, we would like to examine whether Notch signaling pathway is involved in this degradation process. Neural fate specification requires dramatic changes in gene expression patterns. Chromatin remodeling complex has been shown to inhibit neural fate specification in ES organ development, thus, its activity has to be repressed in neural cells. We found that BAP60, a core component of Drosophila chromatin remodeling complex, specifically interacts with Phyl by yeast two-hybrid screening. Thus, we propose to examine whether Phyl inhibits chromatin remodeling complex in neural cells by degrading the BAP60 protein.

Project ID:PA9709-1228
External Project ID:NSC97-2311-B182-002-MY3