Kearsey SE, et al. (2007) Fission yeast Cut8 is required for the repair of DNA double-strand breaks, ribosomal DNA maintenance, and cell survival in the absence of Rqh1 helicase. Mol Cell Biol 27(5):1558-67
Abstract: Schizosaccharomyces pombe Rqh1 is a member of the RecQ DNA helicase family. Members of this protein family are mutated in cancer predisposition diseases, causing Bloom's, Werner, and Rothmund-Thomson syndromes. Rqh1 forms a complex with topoisomerase III and is proposed to process or disrupt aberrant recombination structures that arise during S-phase to allow proper chromosome segregation during mitosis. Intriguingly, in the absence of Rqh1, processing of these structures appears to be dependent on Rad3 (human ATR) in a manner that is distinct from its role in checkpoint control. Here we show that rad3 rqh1 mutants are normally committed to a lethal pathway of DNA repair requiring homologous recombination, but blocking this pathway by Rhp51 inactivation restores viability. Remarkably, viability is also restored by over-expression of Cut8, a nuclear envelope protein involved in tethering and proper function of the proteasome. In keeping with a recently described function of proteasome in the repair of DNA double-strand breaks, we found that Cut8 is also required for DNA double-strand breaks repair and is essential for proper chromosome segregation in the absence of Rqh1, suggesting these proteins might function in a common pathway in homologous recombination repair to ensure accurate nuclear division in S. pombe.
|Status: Published||Type: Journal Article||PubMed ID: 17178839|
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