BRCA2 in mitotic exit: a new role in regulating genomic stability.
Evaluation of: Daniels MJ, Wang Y, Lee M, Venkitaraman AR: Abnormal cytokinesis in cells deficient in the breast cancer susceptibility protein BRCA2. Science 306, 876-879 (2004). Cytokinesis is the division of the cytoplasm of a parent cell into daughter cells after nuclear division. Cytokinesis failure is often accompanied by the generation of cells with an unstable tetraploidy content, which predisposes the cells to develop aneuploidy and malignancies. A recent study by Venkitaraman's group demonstrates that BRCA2, a breast cancer susceptibility gene product, also functions in mediating normal cytokinesis. Similar to the subcellular localization of Aurora kinase, BRCA2 is present at the cleavage furrow and the midbody during late mitosis. Deficiency in BRCA2 function results in cytokinesis failure, which is associated with abnormal localization of myosin II, a key protein essential for the formation of the cleavage furrow. This study is of significance as it shows for the first time that BRCA2 has a function in controlling mitotic exit, deregulation of which contributes to gross genomic instabilities in daughter cells.
Division of Molecular Carcinogenesis, Department of Medicine, New York Medical College, Valhalla, NY 10595, USA.
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D000818:Animals; D024682:BRCA2 Protein / Q000235:genetics* / Q000502:physiology; D020022:Genetic Predisposition to Disease; D042822:Genomic Instability; D006801:Humans; D008938:Mitosis; D009154:Mutation; D009369:Neoplasms / Q000209:etiology / Q000235:genetics
D024682:BRCA2 Protein