Transcriptional control of epidermal cell shape in the Drosophila embryo

Abstract

During development, morphogenetic processes require the integration of numerous signals to properly shape cells and tissues. These signals are interpreted by cells to induce the precise transcriptional circuitry that controls morphogenesis. In the fly embryonic epidermis, the fly Wnt, wingless (wg), generates naked cuticle zones that separate the ventral denticle belts by repressing expression of shavenbaby (svb), which encodes a transcription factor required for denticle formation. What is not known is how Wg and Svb interact to produce the stereotyped diversity of denticle shapes within each belt. One possibility is that graded levels of Svb, responding to graded levels of Wg signaling, determine denticle shape. Indeed, we found that the svb promoter responds differentially to altered Wg activity levels. However, artificially increasing the levels of ectopic svb does not produce morphologically distinct denticles, suggesting that additional factors are involved. We have discovered that a second Wg-responsive transcription factor, encoded by SoxNeuro (SoxN), cooperates with Svb to shape the denticles. Co-expressing SoxN with svb is sufficient to rescue the morphology of denticles in an ectopic location. Furthermore, embryos that lack Svb activity retain the ability to produce a small number of rounded, reduced ventral denticles, due to SoxN activity. We found that svb;SoxN double mutant embryos secrete cuticles that completely lack ventral denticles and dorsal hairs. We also found that a group of known Svb target genes belonging to the zona pellucida family of proteins are differentially activated by SoxN. Finally, we discovered two novel target genes of SoxN, CG16885 and CG30101, which are expressed in denticle-producing cells and which are regulated independently of Svb. SoxN was shown previously to down-regulate Wg signaling and to promote expression of svb. Here, we propose that SoxN acts with Svb, in an additional, direct role, to promote denticle morphogenesis.