Publication

Multiple Rad52-Mediated Homology-Directed Repair Mechanisms Are Required to Prevent Telomere Attrition-Induced Senescence in Saccharomyces cerevisiae

Claussin, C. & Chang, M., Jul-2016, In : PLoS genetics. 12, 7, 19 p., 1006176.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Claussin, C., & Chang, M. (2016). Multiple Rad52-Mediated Homology-Directed Repair Mechanisms Are Required to Prevent Telomere Attrition-Induced Senescence in Saccharomyces cerevisiae. PLoS genetics, 12(7), [1006176]. https://doi.org/10.1371/journal.pgen.1006176

Author

Claussin, Clémence ; Chang, Michael. / Multiple Rad52-Mediated Homology-Directed Repair Mechanisms Are Required to Prevent Telomere Attrition-Induced Senescence in Saccharomyces cerevisiae. In: PLoS genetics. 2016 ; Vol. 12, No. 7.

Harvard

Claussin, C & Chang, M 2016, 'Multiple Rad52-Mediated Homology-Directed Repair Mechanisms Are Required to Prevent Telomere Attrition-Induced Senescence in Saccharomyces cerevisiae', PLoS genetics, vol. 12, no. 7, 1006176. https://doi.org/10.1371/journal.pgen.1006176

Standard

Multiple Rad52-Mediated Homology-Directed Repair Mechanisms Are Required to Prevent Telomere Attrition-Induced Senescence in Saccharomyces cerevisiae. / Claussin, Clémence; Chang, Michael.

In: PLoS genetics, Vol. 12, No. 7, 1006176, 07.2016.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Claussin C, Chang M. Multiple Rad52-Mediated Homology-Directed Repair Mechanisms Are Required to Prevent Telomere Attrition-Induced Senescence in Saccharomyces cerevisiae. PLoS genetics. 2016 Jul;12(7). 1006176. https://doi.org/10.1371/journal.pgen.1006176


BibTeX

@article{f25c36862c3c46e1bb1fde322597f85d,
title = "Multiple Rad52-Mediated Homology-Directed Repair Mechanisms Are Required to Prevent Telomere Attrition-Induced Senescence in Saccharomyces cerevisiae",
abstract = "Most human somatic cells express insufficient levels of telomerase, which can result in telomere shortening and eventually senescence, both of which are hallmarks of ageing. Homology-directed repair (HDR) is important for maintaining proper telomere function in yeast and mammals. In Saccharomyces cerevisiae, Rad52 is required for almost all HDR mechanisms, and telomerase-null cells senesce faster in the absence of Rad52. However, its role in preventing accelerated senescence has been unclear. In this study, we make use of rad52 separation-of-function mutants to find that multiple Rad52-mediated HDR mechanisms are required to delay senescence, including break-induced replication and sister chromatid recombination. In addition, we show that misregulation of histone 3 lysine 56 acetylation, which is known to be defective in sister chromatid recombination, also causes accelerated senescence. We propose a model where Rad52 is needed to repair telomere attrition-induced replication stress.",
keywords = "BREAK-INDUCED REPLICATION, DOUBLE-STRAND BREAKS, POSTREPLICATION REPAIR, MITOTIC RECOMBINATION, LENGTH HOMEOSTASIS, H3K56 ACETYLATION, REPEAT DIVERGENCE, GENOME INTEGRITY, DNA-REPLICATION, YEAST TELOMERES",
author = "Cl{\'e}mence Claussin and Michael Chang",
year = "2016",
month = "7",
doi = "10.1371/journal.pgen.1006176",
language = "English",
volume = "12",
journal = "PLoS genetics",
issn = "1553-7390",
publisher = "PUBLIC LIBRARY SCIENCE",
number = "7",

}

RIS

TY - JOUR

T1 - Multiple Rad52-Mediated Homology-Directed Repair Mechanisms Are Required to Prevent Telomere Attrition-Induced Senescence in Saccharomyces cerevisiae

AU - Claussin, Clémence

AU - Chang, Michael

PY - 2016/7

Y1 - 2016/7

N2 - Most human somatic cells express insufficient levels of telomerase, which can result in telomere shortening and eventually senescence, both of which are hallmarks of ageing. Homology-directed repair (HDR) is important for maintaining proper telomere function in yeast and mammals. In Saccharomyces cerevisiae, Rad52 is required for almost all HDR mechanisms, and telomerase-null cells senesce faster in the absence of Rad52. However, its role in preventing accelerated senescence has been unclear. In this study, we make use of rad52 separation-of-function mutants to find that multiple Rad52-mediated HDR mechanisms are required to delay senescence, including break-induced replication and sister chromatid recombination. In addition, we show that misregulation of histone 3 lysine 56 acetylation, which is known to be defective in sister chromatid recombination, also causes accelerated senescence. We propose a model where Rad52 is needed to repair telomere attrition-induced replication stress.

AB - Most human somatic cells express insufficient levels of telomerase, which can result in telomere shortening and eventually senescence, both of which are hallmarks of ageing. Homology-directed repair (HDR) is important for maintaining proper telomere function in yeast and mammals. In Saccharomyces cerevisiae, Rad52 is required for almost all HDR mechanisms, and telomerase-null cells senesce faster in the absence of Rad52. However, its role in preventing accelerated senescence has been unclear. In this study, we make use of rad52 separation-of-function mutants to find that multiple Rad52-mediated HDR mechanisms are required to delay senescence, including break-induced replication and sister chromatid recombination. In addition, we show that misregulation of histone 3 lysine 56 acetylation, which is known to be defective in sister chromatid recombination, also causes accelerated senescence. We propose a model where Rad52 is needed to repair telomere attrition-induced replication stress.

KW - BREAK-INDUCED REPLICATION

KW - DOUBLE-STRAND BREAKS

KW - POSTREPLICATION REPAIR

KW - MITOTIC RECOMBINATION

KW - LENGTH HOMEOSTASIS

KW - H3K56 ACETYLATION

KW - REPEAT DIVERGENCE

KW - GENOME INTEGRITY

KW - DNA-REPLICATION

KW - YEAST TELOMERES

U2 - 10.1371/journal.pgen.1006176

DO - 10.1371/journal.pgen.1006176

M3 - Article

VL - 12

JO - PLoS genetics

JF - PLoS genetics

SN - 1553-7390

IS - 7

M1 - 1006176

ER -

ID: 34562868