DROSOPHILA NOTCH RECEPTOR ACTIVITY SUPPRESSES HAIRLESS FUNCTION DURING ADULT EXTERNAL SENSORY ORGAN DEVELOPMENT

The neurogenic Notch locus of Drosophila encodes a receptor necessary for cell fate decisions within equivalence groups, such as proneural c lusters. Specification of alternate fates within clusters results from inhibitory communication among cells having comparable neural fate po tential. Genetically, Hairless (H) acts as an antagonist of most neuro genic genes and may insulate neural precursor cells from inhibition. H function is required for commitment to the bristle sensory organ prec ursor (SOP) cell fate and for daughter cell fates. Using Notch gain-of -function alleles and conditional expression of an activated Notch tra nsgene, we show that enhanced signaling produces H-like loss-of-functi on phenotypes by suppressing bristle SOP cell specification or by caus ing an H-like transformation of sensillum daughter cell fates. Further more, adults carrying Notch gain of function and H alleles exhibit syn ergistic enhancement of mutant phenotypes. Over-expression of an H+ tr ansgene product suppressed virtually all phenotypes generated by Notch gain-of-function genotypes. Phenotypes resulting from over-expression of the H+ transgene were blocked by the Notch gain-of-function produc ts, indicating a balance between Notch and H activity. The results sug gest that H insulates SOP cells from inhibition and indicate that H ac tivity is suppressed by Notch signaling.