ArticleMolecular and cellular biology2004
Kinetochores prevent repair of UV damage in Saccharomyces cerevisiae centromeres.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- SWI/SNF-like chromatin remodeling factor Fun30 supports point centromere function in S. cerevisiae.PLoS genetics · 2012Article
- Evidence that the histone methyltransferase Dot1 mediates global genomic repair by methylating histone H3 on lysine 79.The Journal of biological chemistry · 2011Article
- Rapid accessibility of nucleosomal DNA in yeast on a second time scale.The EMBO journal · 2006Article
- UV irradiation stimulates histone acetylation and chromatin remodeling at a repressed yeast locus.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Current awareness on yeast.Yeast (Chichester, England) · 2005Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Centromeres form specialized chromatin structures termed kinetochores which are required for accurate segregation of chromosomes. DNA lesions might disrupt protein-DNA interactions, thereby compromising segregation and genome stability. We show that yeast centromeres are heavily resistant to removal of UV-induced DNA lesions by two different repair systems, photolyase and nucleotide excision repair. Repair resistance persists in G(1)- and G(2)/M-arrested cells. Efficient repair was obtained only by disruption of the kinetochore structure in a ndc10-1 mutant, but not in cse4-1 and cbf1 Delta mutants. Moreover, UV photofootprinting and DNA repair footprinting showed that centromere proteins cover about 120 bp of the centromere elements CDEII and CDEIII, including 20 bp of flanking CDEIII. Thus, DNA lesions do not appear to disrupt protein-DNA interactions in the centromere. Maintaining a stable kinetochore structure seems to be more important for the cell than immediate removal of DNA lesions. It is conceivable that centromeres are repaired by postreplication repair pathways.
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Registered trials
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