【目的】 黑腹果蝇Drosophila melanogaster感觉器官前体细胞（Sensory organ precursors，SOP）的发育依次受预模式基因、原神经基因和神经源性基因的调控，SOP调控基因的功能失常可导致异位SOP表型。cullin-2（cul-2）基因下调引发一种新型异位SOP表型，本研究旨在探究该基因在SOP发生中的作用。【方法】 通过RNA干扰、X-gal染色、免疫组织化学染色和原位杂交来验证翅成虫盘中基因表达模式。【结果】 果蝇cul-2基因抑制果蝇翅成虫盘中SOP形成，且其机制与传统SOP调控基因不同：敲低翅成虫盘中cul-2会导致异位SOP的形成，这些异位SOP在空间上呈连续分布，且不局限于内源性原神经簇区域。与cul-2相关的异位SOP的形成需要原神经基因scute的激活，上调Notch（N）信号通路抑制了与cul-2相关的异位SOP形成，而敲低N信号通路对cul-2表达没有影响，表明在cul-2相关的异位SOP形成中N信号通路没有被激活。而在cul-2敲低后，N信号通路的配体Delta（Dl）的表达未被上调，可解释N信号通路为何未被激活。【结论】 本研究揭示了cul-2在果蝇翅成虫盘细胞中抑制神经源性命运的新功能。

 [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.