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PARP is activated at stalled forks to mediate Mre11-dependent replication restart and recombination.

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PARP is activated at stalled forks to mediate Mre11-dependent replication restart and recombination. / Bryant, Helen E; Petermann, Eva; Schultz, Niklas; Jemth, Ann-Sofie; Loseva, Olga; Issaeva, Natalia; Johansson, Fredrik; Fernandez, Serena; McGlynn, Peter; Helleday, Thomas.

in: EMBO J, Jahrgang 28, Nr. 17, 17, 2009, S. 2601-2615.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Bryant, HE, Petermann, E, Schultz, N, Jemth, A-S, Loseva, O, Issaeva, N, Johansson, F, Fernandez, S, McGlynn, P & Helleday, T 2009, 'PARP is activated at stalled forks to mediate Mre11-dependent replication restart and recombination.', EMBO J, Jg. 28, Nr. 17, 17, S. 2601-2615. <http://www.ncbi.nlm.nih.gov/pubmed/19629035?dopt=Citation>

APA

Bryant, H. E., Petermann, E., Schultz, N., Jemth, A-S., Loseva, O., Issaeva, N., Johansson, F., Fernandez, S., McGlynn, P., & Helleday, T. (2009). PARP is activated at stalled forks to mediate Mre11-dependent replication restart and recombination. EMBO J, 28(17), 2601-2615. [17]. http://www.ncbi.nlm.nih.gov/pubmed/19629035?dopt=Citation

Vancouver

Bryant HE, Petermann E, Schultz N, Jemth A-S, Loseva O, Issaeva N et al. PARP is activated at stalled forks to mediate Mre11-dependent replication restart and recombination. EMBO J. 2009;28(17):2601-2615. 17.

Bibtex

@article{230e8be3b8dc4f719e84335e7d332e21,
title = "PARP is activated at stalled forks to mediate Mre11-dependent replication restart and recombination.",
abstract = "If replication forks are perturbed, a multifaceted response including several DNA repair and cell cycle checkpoint pathways is activated to ensure faithful DNA replication. Here, we show that poly(ADP-ribose) polymerase 1 (PARP1) binds to and is activated by stalled replication forks that contain small gaps. PARP1 collaborates with Mre11 to promote replication fork restart after release from replication blocks, most likely by recruiting Mre11 to the replication fork to promote resection of DNA. Both PARP1 and PARP2 are required for hydroxyurea-induced homologous recombination to promote cell survival after replication blocks. Together, our data suggest that PARP1 and PARP2 detect disrupted replication forks and attract Mre11 for end processing that is required for subsequent recombination repair and restart of replication forks.",
author = "Bryant, {Helen E} and Eva Petermann and Niklas Schultz and Ann-Sofie Jemth and Olga Loseva and Natalia Issaeva and Fredrik Johansson and Serena Fernandez and Peter McGlynn and Thomas Helleday",
year = "2009",
language = "Deutsch",
volume = "28",
pages = "2601--2615",
journal = "EMBO J",
issn = "0261-4189",
publisher = "NATURE PUBLISHING GROUP",
number = "17",

}

RIS

TY - JOUR

T1 - PARP is activated at stalled forks to mediate Mre11-dependent replication restart and recombination.

AU - Bryant, Helen E

AU - Petermann, Eva

AU - Schultz, Niklas

AU - Jemth, Ann-Sofie

AU - Loseva, Olga

AU - Issaeva, Natalia

AU - Johansson, Fredrik

AU - Fernandez, Serena

AU - McGlynn, Peter

AU - Helleday, Thomas

PY - 2009

Y1 - 2009

N2 - If replication forks are perturbed, a multifaceted response including several DNA repair and cell cycle checkpoint pathways is activated to ensure faithful DNA replication. Here, we show that poly(ADP-ribose) polymerase 1 (PARP1) binds to and is activated by stalled replication forks that contain small gaps. PARP1 collaborates with Mre11 to promote replication fork restart after release from replication blocks, most likely by recruiting Mre11 to the replication fork to promote resection of DNA. Both PARP1 and PARP2 are required for hydroxyurea-induced homologous recombination to promote cell survival after replication blocks. Together, our data suggest that PARP1 and PARP2 detect disrupted replication forks and attract Mre11 for end processing that is required for subsequent recombination repair and restart of replication forks.

AB - If replication forks are perturbed, a multifaceted response including several DNA repair and cell cycle checkpoint pathways is activated to ensure faithful DNA replication. Here, we show that poly(ADP-ribose) polymerase 1 (PARP1) binds to and is activated by stalled replication forks that contain small gaps. PARP1 collaborates with Mre11 to promote replication fork restart after release from replication blocks, most likely by recruiting Mre11 to the replication fork to promote resection of DNA. Both PARP1 and PARP2 are required for hydroxyurea-induced homologous recombination to promote cell survival after replication blocks. Together, our data suggest that PARP1 and PARP2 detect disrupted replication forks and attract Mre11 for end processing that is required for subsequent recombination repair and restart of replication forks.

M3 - SCORING: Zeitschriftenaufsatz

VL - 28

SP - 2601

EP - 2615

JO - EMBO J

JF - EMBO J

SN - 0261-4189

IS - 17

M1 - 17

ER -