Redundant mechanisms mediate bristle patterning on the Drosophila thorax.

The thoracic bristle pattern of Drosophila results from the spatially restricted expression of the achaete-scute (ac-sc) genes in clusters of cells, mediated by the activity of many discrete cis-regulatory sequences. However, ubiquitous expression of sc or asense (ase) achieved with a heterologous promoter, in the absence of endogenous ac-sc expression, and the activity of the cis-regulatory elements, allows the development of bristles positioned at wild-type locations. We demonstrate that the products of the genes stripe, hairy, and extramacrochaetae contribute to rescue by antagonizing the activity of Sc and Ase. The three genes are expressed in specific but overlapping spatial domains of expression that form a prepattern that allows precise positioning of bristles. The redundant mechanisms might contribute to the robustness of the pattern. We discuss the possibility that patterning in trans by antagonism is ancestral and that the positional cis-regulatory sequences might be of recent origin.

NF-kappaB/Rel-mediated regulation of the neural fate in Drosophila.

Two distinct roles are described for Dorsal, Dif and Relish, the three NF-kappaB/Rel proteins of Drosophila, in the development of the peripheral nervous system. First, these factors regulate transcription of scute during the singling out of sensory organ precursors from clusters of cells expressing the proneural genes achaete and scute. This effect is possibly mediated through binding sites for NF-kappaB/Rel proteins in a regulatory module of the scute gene required for maintenance of scute expression in precursors as well as repression in cells surrounding precursors. Second, genetic evidence suggests that the receptor Toll-8, Relish, Dif and Dorsal, and the caspase Dredd pathway are active over the entire imaginal disc epithelium, but Toll-8 expression is excluded from sensory organ precursors. Relish promotes rapid turnover of transcripts of the target genes scute and asense through an indirect, post-transcriptional mechanism. We propose that this buffering of gene expression levels serves to keep the neuro-epithelium constantly poised for neurogenesis.