Our research aims to understand the gene-regulatory networks which link the specification of cell fates to the morphogenetic events which accompany cell differentiation. Our model system is the development of epidermal appendages, called trichomes, on the ventral site of the Drosophila melanogaster embryo. The Drosophila ventral epidermis displays an invariant pattern of smooth cells and cells which form trichomes. Binary fate specification in the ventral epidermis is achieved by the activities of morphogen signaling cascades which converge onto the transcription factors SoxNeuro (SoxN) and Dichaete (D). Within the epidermis, SoxN/D expression is restricted to trichome-producing cells. Concomitant loss of SoxN and D results in the loss of trichomes while misexpression results in ectopic trichomes indicating that SoxN and D are necessary and sufficient for trichome formation. SoxN and D activate the expression of the transcription factor Shavenbaby (Svb) which in turn regulates the expression of proteins known to act in cell shape re-modelling. Hence, a linear gene-regulatory network appears to control trichome formation with SoxN/D and their target svb as the transcriptional links between signaling cascades and trichome morphogenesis. However, several observations indicate that the functions of SoxN/D are more complex. First, misexpression of either svb or SoxN results in ectopic trichomes with distinct morphologies. Second, SoxN;D mutant embryos do not form any trichomes. By contrast, in svb mutants trichome formation is impaired but not abolished. The remaining trichomes are under the control of SoxN since svb;SoxN double mutant embryos do not form trichomes. Third, misexpression of SoxN in svb mutants results in the formation of trichomes, albeit with aberrant morphology. These results indicate that SoxN can effect epidermal morphogenesis in parallel to svb . We have identified several genes which are regulated by SoxN in the ventral epidermis. These genes include known regulators of actin dynamics, planar cell polarity and other functions. Our results suggest that the gene-regulatory network which underlies trichome morphogenesis in the Drosophila epidermis is not linear.