Similar to the sc SMC-enhancer, the stretches of D. virilis conserved DNA contain E boxes, one N box, two alpha boxes, and one beta box, supporting the relevance of these boxes for SMC enhancer function. Moreover, the neurogenic gene Bearded, which is expressed in proneural clusters and SMCs, contains in its regulatory region one E box, necessary for its expression, and one motif identical to the alpha2 box. Notch signaling prevents more than one of a proneural cluster from becoming SMCs. To distinguish among these alternatives, an examination was carried out of the activity promoted by each type of enhancer, in both wild-type and in N ts discs. N inactivation allows the SMC enhancer to drive expression in many cells of proneural clusters.
Expression can occur in contiguous cells, indicating the failure of lateral inhibition.
This correlates with the SMCs being the cells that signal maximally and inhibit their neighbors from acquiring the neural fate, while the SMCs themselves are not inhibited. However, overexpression with presumably stronger GAL4 drivers does interfere with ac-sc expression in proneural clusters. Remarkably, the removal of one or both binding sites does not modify the SMC specificity of the enhancer, as might be expected if these binding sites mediated the repression of enhancer function in response to N signaling. A focus was placed on sensory organ precursor determination, wing vein determination and wing pattern formation. During wing patterning, Notch activity orchestrates a complex sequence of events that define the dorsoventral boundary of the wing.