RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand Breaks

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RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand Breaks. / Lu, Huiming; Shamanna, Raghavendra A; Keijzers, Guido; Anand, Roopesh; Rasmussen, Lene Juel; Cejka, Petr; Croteau, Deborah L; Bohr, Vilhelm A.

In: Cell Reports, Vol. 16, No. 1, 28.06.2016, p. 161-173.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Lu, H, Shamanna, RA, Keijzers, G, Anand, R, Rasmussen, LJ, Cejka, P, Croteau, DL & Bohr, VA 2016, 'RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand Breaks', Cell Reports, vol. 16, no. 1, pp. 161-173. https://doi.org/10.1016/j.celrep.2016.05.079

APA

Lu, H., Shamanna, R. A., Keijzers, G., Anand, R., Rasmussen, L. J., Cejka, P., ... Bohr, V. A. (2016). RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand Breaks. Cell Reports, 16(1), 161-173. https://doi.org/10.1016/j.celrep.2016.05.079

Vancouver

Lu H, Shamanna RA, Keijzers G, Anand R, Rasmussen LJ, Cejka P et al. RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand Breaks. Cell Reports. 2016 Jun 28;16(1):161-173. https://doi.org/10.1016/j.celrep.2016.05.079

Author

Lu, Huiming ; Shamanna, Raghavendra A ; Keijzers, Guido ; Anand, Roopesh ; Rasmussen, Lene Juel ; Cejka, Petr ; Croteau, Deborah L ; Bohr, Vilhelm A. / RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand Breaks. In: Cell Reports. 2016 ; Vol. 16, No. 1. pp. 161-173.

Bibtex

@article{5679e27b7a0e484da04c76b7b33daa77,
title = "RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand Breaks",
abstract = "The RecQ helicase RECQL4, mutated in Rothmund-Thomson syndrome, regulates genome stability, aging, and cancer. Here, we identify a crucial role for RECQL4 in DNA end resection, which is the initial and an essential step of homologous recombination (HR)-dependent DNA double-strand break repair (DSBR). Depletion of RECQL4 severely reduces HR-mediated repair and 5' end resection in vivo. RECQL4 physically interacts with MRE11-RAD50-NBS1 (MRN), which senses DSBs and initiates DNA end resection with CtIP. The MRE11 exonuclease regulates the retention of RECQL4 at laser-induced DSBs. RECQL4 also directly interacts with CtIP via its N-terminal domain and promotes CtIP recruitment to the MRN complex at DSBs. Moreover, inactivation of RECQL4's helicase activity impairs DNA end processing and HR-dependent DSBR without affecting its interaction with MRE11 and CtIP, suggesting an important role for RECQL4's unwinding activity in the process. Thus, we report that RECQL4 is an important participant in HR-dependent DSBR.",
author = "Huiming Lu and Shamanna, {Raghavendra A} and Guido Keijzers and Roopesh Anand and Rasmussen, {Lene Juel} and Petr Cejka and Croteau, {Deborah L} and Bohr, {Vilhelm A}",
note = "Published by Elsevier Inc.",
year = "2016",
month = "6",
day = "28",
doi = "10.1016/j.celrep.2016.05.079",
language = "English",
volume = "16",
pages = "161--173",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand Breaks

AU - Lu, Huiming

AU - Shamanna, Raghavendra A

AU - Keijzers, Guido

AU - Anand, Roopesh

AU - Rasmussen, Lene Juel

AU - Cejka, Petr

AU - Croteau, Deborah L

AU - Bohr, Vilhelm A

N1 - Published by Elsevier Inc.

PY - 2016/6/28

Y1 - 2016/6/28

N2 - The RecQ helicase RECQL4, mutated in Rothmund-Thomson syndrome, regulates genome stability, aging, and cancer. Here, we identify a crucial role for RECQL4 in DNA end resection, which is the initial and an essential step of homologous recombination (HR)-dependent DNA double-strand break repair (DSBR). Depletion of RECQL4 severely reduces HR-mediated repair and 5' end resection in vivo. RECQL4 physically interacts with MRE11-RAD50-NBS1 (MRN), which senses DSBs and initiates DNA end resection with CtIP. The MRE11 exonuclease regulates the retention of RECQL4 at laser-induced DSBs. RECQL4 also directly interacts with CtIP via its N-terminal domain and promotes CtIP recruitment to the MRN complex at DSBs. Moreover, inactivation of RECQL4's helicase activity impairs DNA end processing and HR-dependent DSBR without affecting its interaction with MRE11 and CtIP, suggesting an important role for RECQL4's unwinding activity in the process. Thus, we report that RECQL4 is an important participant in HR-dependent DSBR.

AB - The RecQ helicase RECQL4, mutated in Rothmund-Thomson syndrome, regulates genome stability, aging, and cancer. Here, we identify a crucial role for RECQL4 in DNA end resection, which is the initial and an essential step of homologous recombination (HR)-dependent DNA double-strand break repair (DSBR). Depletion of RECQL4 severely reduces HR-mediated repair and 5' end resection in vivo. RECQL4 physically interacts with MRE11-RAD50-NBS1 (MRN), which senses DSBs and initiates DNA end resection with CtIP. The MRE11 exonuclease regulates the retention of RECQL4 at laser-induced DSBs. RECQL4 also directly interacts with CtIP via its N-terminal domain and promotes CtIP recruitment to the MRN complex at DSBs. Moreover, inactivation of RECQL4's helicase activity impairs DNA end processing and HR-dependent DSBR without affecting its interaction with MRE11 and CtIP, suggesting an important role for RECQL4's unwinding activity in the process. Thus, we report that RECQL4 is an important participant in HR-dependent DSBR.

U2 - 10.1016/j.celrep.2016.05.079

DO - 10.1016/j.celrep.2016.05.079

M3 - Journal article

C2 - 27320928

VL - 16

SP - 161

EP - 173

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 1

ER -

ID: 166270617