[Aim]  To investigate the role of the cullin-2 (cul-2) gene in the development of sensory organ precursors (SOPs) in Drosophila melanogaster. [Methods]  Gene expression patterns in the wing imaginal disc were verified by RNA interference, X-gal staining, immunohistochemistry, and in situ hybridization. [Results]  The Drosophila cul-2 gene suppressed SOP formation in the wing imaginal disc via a mechanism different from that used by classical SOP regulatory genes. Knock-down of cul-2 in the wing disc led to the formation of ectopic SOPs, which had a spatially continuous pattern and were not restricted to endogenous, proneural cluster areas. The formation of cul-2-associated ectopic SOPs required the activation of the proneural gene scute. The upregulated Notch (N) signaling pathway suppressed the formation of cul-2-associated ectopic SOPs, whereas knock-down of this pathway had no effect on cul-2 expression, indicating that the N signaling pathway was not activated during the formation of cul-2-associated ectopic SOPs. Moreover, the expression of Delta (Dl), the ligand of the N signaling pathway, was not upregulated after cul-2 knock-down, which may explain why the N signaling pathway was not activated. [Conclusion]  These results reveal a novel function of cul-2 as a suppressor of neurogenic potential in the development of Drosophila wing disc cells.