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InDrosophila , mutation of the oncogeneMyb reduced the expression of mitotic genes, such aspolo andial , and caused multiple mitotic defects, including disrupted chromosome condensation and abnormal spindles. We now show that binucleate cells, the hallmark phenotype of cytokinesis failure, accumulate inMyb -null ovarian follicle cell and wing disc epithelia. Myb functions as an activator in the generally repressiveD rosophilaR BF,E 2F2, andM yb (dREAM)/Myb-MuvB complex. Absence of the dREAM subunit Mip130 or E2F2 suppressed theMyb -null cytokinesis defect. Therefore, we usedMyb -null binucleate cells as a quantitative phenotypic readout of transcriptional repression by the dREAM complex. In the absence of Myb, the complex was sensitive to the dose of the subunits E2F2, Mip120, Caf1, and Lin-52 but not Mip130 or Mip40. Surprisingly, reduction of the dose ofHis2Av /H2A .z also suppressed theMyb -null binucleate cell phenotype, suggesting a novel role for this variant histone in transcriptional repression by the dREAM complex.

The Complex Containing Drosophila Myb and RB/E2F2 Regulates Cytokinesis in a Histone H2Av-Dependent Manner