phyllopod in the fate specification of sensory organ precursor (SOP). H. Pi , S.K. Huang , C.T. Chien. Inst Molec Biol, Academia Sinica, Taipei, Taiwan.

   Each external sensory organ is derived from a single SOP. We showed that phyllopod ( phyl ), originally identified to be essential for R7 photoreceptor differentiation, is required for SOP specification. Loss-of-function mutations in phyl results in failure in SOP formation, which leads to missing bristles in adult flies. Conversely, misexpression of phyl promotes ectopic SOP formation. phyl functions as a genetic switch in specifying the fate of the SOP cells. We found that expression of the proneural gene is not affected in phyl mutants, and misexpression of phyl rescues the bristle-missing defects of the strong achaete-scute mutant sc^10-1, indicating that phyl functions downstream of achaete-scute in SOP specification. phyl is specifically expressed in SOP cells. Promoter analysis showed that 3.4Kb region upstream of phyl translation start site fused to phyl ORF is sufficient to rescue the bristle-missing defect of phyl mutants. We are testing whether phyl is the direct downstream target of proneural proteins. Notch signaling is essential to repress SOP specification. We demonstrate that phyl acts epistatically to Notch , and its mRNA level is negatively regulated by Notch signaling. These results suggest that Notch signaling represses SOP specification by repressing phyl expression. Furthermore, Phyl interacts with Notch in yeast two-hybrid assay and genetically. Ectopic expression of phyl along the A-P boundary of wing disk causes wing vein expansion analogous to disruption of Notch signaling. We are testing how Phyl downregulates Notch activity during SOP specification.