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Recruitment of Rad51 and Rad52 to short telomeres triggers a Mec1-mediated hypersensitivity to double-stranded DNA breaks in senescent budding yeast.
PLoS One. 2009 Dec 14; 4(12):e8224.Plos

Abstract

Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the action of telomerase. In both mammalian tumor and yeast cells that lack telomerase, telomeres are maintained by an alternative recombination mechanism. Here we demonstrated that the budding yeast Saccharomyces cerevisiae type I survivors derived from telomerase-deficient cells were hypersensitive to DNA damaging agents. Assays to track telomere lengths and drug sensitivity of telomerase-deficient cells from spore colonies to survivors suggested a correlation between telomere shortening and bleomycin sensitivity. Our genetic studies demonstrated that this sensitivity depends on Mec1, which signals checkpoint activation, leading to prolonged cell-cycle arrest in senescent budding yeasts. Moreover, we also observed that when cells equipped with short telomeres, recruitments of homologous recombination proteins, Rad51 and Rad52, were reduced at an HO-endonuclease-catalyzed double-strand break (DSB), while their associations were increased at chromosome ends. These results suggested that the sensitive phenotype may be attributed to the sequestration of repair proteins to compromised telomeres, thus limiting the repair capacity at bona fide DSB sites.

Authors+Show Affiliations

Department of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20011546

Citation

Lin, Yi-Hsuan, et al. "Recruitment of Rad51 and Rad52 to Short Telomeres Triggers a Mec1-mediated Hypersensitivity to Double-stranded DNA Breaks in Senescent Budding Yeast." PloS One, vol. 4, no. 12, 2009, pp. e8224.
Lin YH, Chang CC, Wong CW, et al. Recruitment of Rad51 and Rad52 to short telomeres triggers a Mec1-mediated hypersensitivity to double-stranded DNA breaks in senescent budding yeast. PLoS One. 2009;4(12):e8224.
Lin, Y. H., Chang, C. C., Wong, C. W., & Teng, S. C. (2009). Recruitment of Rad51 and Rad52 to short telomeres triggers a Mec1-mediated hypersensitivity to double-stranded DNA breaks in senescent budding yeast. PloS One, 4(12), e8224. https://doi.org/10.1371/journal.pone.0008224
Lin YH, et al. Recruitment of Rad51 and Rad52 to Short Telomeres Triggers a Mec1-mediated Hypersensitivity to Double-stranded DNA Breaks in Senescent Budding Yeast. PLoS One. 2009 Dec 14;4(12):e8224. PubMed PMID: 20011546.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Recruitment of Rad51 and Rad52 to short telomeres triggers a Mec1-mediated hypersensitivity to double-stranded DNA breaks in senescent budding yeast. AU - Lin,Yi-Hsuan, AU - Chang,Chia-Ching, AU - Wong,Chui-Wei, AU - Teng,Shu-Chun, Y1 - 2009/12/14/ PY - 2009/10/17/received PY - 2009/11/16/accepted PY - 2009/12/17/entrez PY - 2009/12/17/pubmed PY - 2010/3/18/medline SP - e8224 EP - e8224 JF - PloS one JO - PLoS One VL - 4 IS - 12 N2 - Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the action of telomerase. In both mammalian tumor and yeast cells that lack telomerase, telomeres are maintained by an alternative recombination mechanism. Here we demonstrated that the budding yeast Saccharomyces cerevisiae type I survivors derived from telomerase-deficient cells were hypersensitive to DNA damaging agents. Assays to track telomere lengths and drug sensitivity of telomerase-deficient cells from spore colonies to survivors suggested a correlation between telomere shortening and bleomycin sensitivity. Our genetic studies demonstrated that this sensitivity depends on Mec1, which signals checkpoint activation, leading to prolonged cell-cycle arrest in senescent budding yeasts. Moreover, we also observed that when cells equipped with short telomeres, recruitments of homologous recombination proteins, Rad51 and Rad52, were reduced at an HO-endonuclease-catalyzed double-strand break (DSB), while their associations were increased at chromosome ends. These results suggested that the sensitive phenotype may be attributed to the sequestration of repair proteins to compromised telomeres, thus limiting the repair capacity at bona fide DSB sites. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/20011546/Recruitment_of_Rad51_and_Rad52_to_short_telomeres_triggers_a_Mec1_mediated_hypersensitivity_to_double_stranded_DNA_breaks_in_senescent_budding_yeast_ L2 - https://dx.plos.org/10.1371/journal.pone.0008224 DB - PRIME DP - Unbound Medicine ER -