Cell cycle-regulated centers of DNA double-strand break repair

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Cell cycle-regulated centers of DNA double-strand break repair. / Lisby, Michael; Antúnez de Mayolo, Adriana; Mortensen, Uffe H; Rothstein, Rodney.

I: Cell Cycle, Bind 2, Nr. 5, 10.09.2003, s. 479-83.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Lisby, M, Antúnez de Mayolo, A, Mortensen, UH & Rothstein, R 2003, 'Cell cycle-regulated centers of DNA double-strand break repair', Cell Cycle, bind 2, nr. 5, s. 479-83.

APA

Lisby, M., Antúnez de Mayolo, A., Mortensen, U. H., & Rothstein, R. (2003). Cell cycle-regulated centers of DNA double-strand break repair. Cell Cycle, 2(5), 479-83.

Vancouver

Lisby M, Antúnez de Mayolo A, Mortensen UH, Rothstein R. Cell cycle-regulated centers of DNA double-strand break repair. Cell Cycle. 2003 sep. 10;2(5):479-83.

Author

Lisby, Michael ; Antúnez de Mayolo, Adriana ; Mortensen, Uffe H ; Rothstein, Rodney. / Cell cycle-regulated centers of DNA double-strand break repair. I: Cell Cycle. 2003 ; Bind 2, Nr. 5. s. 479-83.

Bibtex

@article{713f8864497d4aa59c0b108a9bf6dfea,
title = "Cell cycle-regulated centers of DNA double-strand break repair",
abstract = "In eukaryotes, homologous recombination is an important pathway for the repair of DNA double-strand breaks. We have studied this process in living cells in the yeast Saccharomyces cerevisiae using Rad52 as a cell biological marker. In response to DNA damage, Rad52 redistributes itself and forms foci specifically during S phase. We have shown previously that Rad52 foci are centers of DNA repair where multiple DNA double-strand breaks colocalize. Here we report a correlation between the timing of Rad52 focus formation and modification of the Rad52 protein. In addition, we show that the two ends of a double-strand break are held tightly together in the majority of cells. Interestingly, in a small but significant fraction of the S phase cells, the two ends of a break separate suggesting that mechanisms exist to reassociate and align these ends for proper DNA repair.",
keywords = "Cell Cycle, DNA Damage, DNA Repair, DNA-Binding Proteins, Rad52 DNA Repair and Recombination Protein, Recombination, Genetic, S Phase, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.",
author = "Michael Lisby and {Ant{\'u}nez de Mayolo}, Adriana and Mortensen, {Uffe H} and Rodney Rothstein",
year = "2003",
month = sep,
day = "10",
language = "English",
volume = "2",
pages = "479--83",
journal = "Cell Cycle",
issn = "1538-4101",
publisher = "Taylor & Francis",
number = "5",

}

RIS

TY - JOUR

T1 - Cell cycle-regulated centers of DNA double-strand break repair

AU - Lisby, Michael

AU - Antúnez de Mayolo, Adriana

AU - Mortensen, Uffe H

AU - Rothstein, Rodney

PY - 2003/9/10

Y1 - 2003/9/10

N2 - In eukaryotes, homologous recombination is an important pathway for the repair of DNA double-strand breaks. We have studied this process in living cells in the yeast Saccharomyces cerevisiae using Rad52 as a cell biological marker. In response to DNA damage, Rad52 redistributes itself and forms foci specifically during S phase. We have shown previously that Rad52 foci are centers of DNA repair where multiple DNA double-strand breaks colocalize. Here we report a correlation between the timing of Rad52 focus formation and modification of the Rad52 protein. In addition, we show that the two ends of a double-strand break are held tightly together in the majority of cells. Interestingly, in a small but significant fraction of the S phase cells, the two ends of a break separate suggesting that mechanisms exist to reassociate and align these ends for proper DNA repair.

AB - In eukaryotes, homologous recombination is an important pathway for the repair of DNA double-strand breaks. We have studied this process in living cells in the yeast Saccharomyces cerevisiae using Rad52 as a cell biological marker. In response to DNA damage, Rad52 redistributes itself and forms foci specifically during S phase. We have shown previously that Rad52 foci are centers of DNA repair where multiple DNA double-strand breaks colocalize. Here we report a correlation between the timing of Rad52 focus formation and modification of the Rad52 protein. In addition, we show that the two ends of a double-strand break are held tightly together in the majority of cells. Interestingly, in a small but significant fraction of the S phase cells, the two ends of a break separate suggesting that mechanisms exist to reassociate and align these ends for proper DNA repair.

KW - Cell Cycle

KW - DNA Damage

KW - DNA Repair

KW - DNA-Binding Proteins

KW - Rad52 DNA Repair and Recombination Protein

KW - Recombination, Genetic

KW - S Phase

KW - Saccharomyces cerevisiae

KW - Saccharomyces cerevisiae Proteins

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

KW - Research Support, U.S. Gov't, P.H.S.

M3 - Journal article

C2 - 12963848

VL - 2

SP - 479

EP - 483

JO - Cell Cycle

JF - Cell Cycle

SN - 1538-4101

IS - 5

ER -

ID: 184396723