Repression by Su-H complexes may act in parallel to other regulatory mechanisms to inhibit the expression of Notch target genes in SOPs. For instance, the transcriptional repressor Longitudinal lacking was shown to repress the expression of Notch target genes, and to genetically interact with H during adult peripheral neurogenesis. Additionally,BMN673 the nuclear BEN-solo family protein Insensitive was recently shown to directly interact with Su and to inhibit in a H-independent manner the expression of Notch target genes, both in embryos and in a cell-based assay. This CSL co-repressor activity appears to be conserved in mammals since BEND6, a mouse homolog of Insv, binds CSL and antagonizes Notch-dependent gene expression in neural cells. Of note, both Lola and Insv appear to be expressed at higher levels in SOPs, indicating that repression of Notch target genes is achieved by several mechanisms in this developmental context. We next used a gain-of-function approach to further examine the function of the insb gene. To do so, we generated a UAS-Insb-GFP transgene. The ectopic expression of the Insb-GFP protein was then achieved using various Gal4 drivers. Using pannier-Gal4, we found that over-expression of Insb-GFP resulted in a bristle loss phenotype. This balding phenotype was associated with both an increased density of sensory organs in the dorso-central region of the notum that expressed pnr-Gal4 and an increased number of Elav-positive neurons. Hence, we propose that overexpression of Insb-GFP led first to the specification of too many SOPs, hence the increased number of external sensory organs, and second to the transformation of external cells into internal cells, notably neurons,Bortezomib leading to the balding phenotype seen in adult flies. Thus, this insb gain-of-function generated a lateral inhibition and cell fate transformation phenotypes similar to the ones observed upon loss of Notch activity. We therefore propose that the insb gene encodes a nuclear antagonist of Notch. To further test this proposal, we analysed the effect of insb over-expression on another Notch-dependent process. The develop-ment of the wing involves the activation of Notch at the wing margin.