Myb controls G 2 /M progression by inducing cyclin B expression in the Drosophila eye imaginal disc

The c‐ myb proto‐oncogene product (c‐Myb) is a transcriptional activator. Vertebrate c‐Myb is a key regulator of the G 1 /S transition in cell cycle, while Drosophila Myb (dMyb) is important for the G 2 /M transition. Here we report that dMyb induces expression of cyclin B, a critical regulator of the G 2 /M transition, in Drosophila eye imaginal disc. In the wild‐type eye disc, dmyb mRNA was expressed in the stripes both anterior and posterior to the morphogenetic furrow. Ectopic expression of C‐terminal‐truncated dMyb in the eye disc caused ectopic expression of cyclin B and the rough eye phenotype. This rough eye phenotype correlated with prolonged M phase, caused by overexpression of cyclin B. Cyclin B expression was lost in dmyb ‐deficient clones. In Schneider cells, the activity of the cyclin B promoter was dramatically reduced by loss of dMyb using the RNA interference method. Mutations of the multiple AACNG sequences in the cyclin B promoter also abolished the promoter activity. These results indicate that dMyb regulates the G 2 /M transition by inducing cyclin B expression via binding to its promoter.