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Fig. 7. Model of cell fate specification during lateral inhibition in PNCs. (A) In wild-type SOPs (right), which do not respond to the Dl/N signal, Su(H) is in its default repressive state, linked via H to the co-repressors Gro and CtBP. It is bound directly to high-affinity sites in SOP-inhibitory target genes in the E(spl)-C, and prevents activation of these genes by the high proneural protein levels prevailing in that cell. The proneural proteins are thus free to activate genes that promote the SOP fate. In wild-type non-SOPs (left), activation of the N receptor associates Su(H) with a transcriptional activation complex that includes N^IC and Mam. In this activated state, Su(H) synergizes with the proneural proteins to directly activate expression of the same SOP-inhibitory genes, committing the cell to an epidermal fate. (B) In the absence of direct repression by Su(H) [e.g. by mutation of Su(H)-binding sites (Sm)], SOP-inhibitory genes of the E(spl)-C are ectopically activated in the SOP by the high levels of proneural proteins, which can drive the cell to adopt an inappropriate epidermal fate. In this model, three key regulators – the proneural proteins, Su(H) and Gro – each have transcriptional regulatory activities that are oppositely directed, with respect to cell fate, in SOPs versus non-SOPs. All three function both to promote and to inhibit the SOP fate during lateral inhibition.

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