Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination.

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Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination. / Alvaro, David; Lisby, Michael; Rothstein, Rodney.

In: PLoS Genetics, Vol. 3, No. 12, 2007, p. e228.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Alvaro, D, Lisby, M & Rothstein, R 2007, 'Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination.', PLoS Genetics, vol. 3, no. 12, pp. e228. https://doi.org/10.1371/journal.pgen.0030228

APA

Alvaro, D., Lisby, M., & Rothstein, R. (2007). Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination. PLoS Genetics, 3(12), e228. https://doi.org/10.1371/journal.pgen.0030228

Vancouver

Alvaro D, Lisby M, Rothstein R. Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination. PLoS Genetics. 2007;3(12):e228. https://doi.org/10.1371/journal.pgen.0030228

Author

Alvaro, David ; Lisby, Michael ; Rothstein, Rodney. / Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination. In: PLoS Genetics. 2007 ; Vol. 3, No. 12. pp. e228.

Bibtex

@article{57c4ce00124211ddbee902004c4f4f50,
title = "Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination.",
abstract = "To investigate the DNA damage response, we undertook a genome-wide study in Saccharomyces cerevisiae and identified 86 gene deletions that lead to increased levels of spontaneous Rad52 foci in proliferating diploid cells. More than half of the genes are conserved across species ranging from yeast to humans. Along with genes involved in DNA replication, repair, and chromatin remodeling, we found 22 previously uncharacterized open reading frames. Analysis of recombination rates and synthetic genetic interactions with rad52Delta suggests that multiple mechanisms are responsible for elevated levels of spontaneous Rad52 foci, including increased production of recombinogenic lesions, sister chromatid recombination defects, and improper focus assembly/disassembly. Our cell biological approach demonstrates the diversity of processes that converge on homologous recombination, protect against spontaneous DNA damage, and facilitate efficient repair.",
author = "David Alvaro and Michael Lisby and Rodney Rothstein",
year = "2007",
doi = "10.1371/journal.pgen.0030228",
language = "English",
volume = "3",
pages = "e228",
journal = "P L o S Genetics",
issn = "1553-7390",
publisher = "Public Library of Science",
number = "12",

}

RIS

TY - JOUR

T1 - Genome-wide analysis of Rad52 foci reveals diverse mechanisms impacting recombination.

AU - Alvaro, David

AU - Lisby, Michael

AU - Rothstein, Rodney

PY - 2007

Y1 - 2007

N2 - To investigate the DNA damage response, we undertook a genome-wide study in Saccharomyces cerevisiae and identified 86 gene deletions that lead to increased levels of spontaneous Rad52 foci in proliferating diploid cells. More than half of the genes are conserved across species ranging from yeast to humans. Along with genes involved in DNA replication, repair, and chromatin remodeling, we found 22 previously uncharacterized open reading frames. Analysis of recombination rates and synthetic genetic interactions with rad52Delta suggests that multiple mechanisms are responsible for elevated levels of spontaneous Rad52 foci, including increased production of recombinogenic lesions, sister chromatid recombination defects, and improper focus assembly/disassembly. Our cell biological approach demonstrates the diversity of processes that converge on homologous recombination, protect against spontaneous DNA damage, and facilitate efficient repair.

AB - To investigate the DNA damage response, we undertook a genome-wide study in Saccharomyces cerevisiae and identified 86 gene deletions that lead to increased levels of spontaneous Rad52 foci in proliferating diploid cells. More than half of the genes are conserved across species ranging from yeast to humans. Along with genes involved in DNA replication, repair, and chromatin remodeling, we found 22 previously uncharacterized open reading frames. Analysis of recombination rates and synthetic genetic interactions with rad52Delta suggests that multiple mechanisms are responsible for elevated levels of spontaneous Rad52 foci, including increased production of recombinogenic lesions, sister chromatid recombination defects, and improper focus assembly/disassembly. Our cell biological approach demonstrates the diversity of processes that converge on homologous recombination, protect against spontaneous DNA damage, and facilitate efficient repair.

U2 - 10.1371/journal.pgen.0030228

DO - 10.1371/journal.pgen.0030228

M3 - Journal article

C2 - 18085829

VL - 3

SP - e228

JO - P L o S Genetics

JF - P L o S Genetics

SN - 1553-7390

IS - 12

ER -

ID: 3802227