A Role for BLM in Double-Strand Break Repair Pathway Choice: Prevention of CtIP/Mre11-Mediated Alternative Nonhomologous End-Joining.

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

A Role for BLM in Double-Strand Break Repair Pathway Choice: Prevention of CtIP/Mre11-Mediated Alternative Nonhomologous End-Joining. / Grabarz, Anastazja ; Guirouilh-Barbat, Josée ; Barascu, Aurelia ; Pennarun, Gaëlle; Genet, Diane ; Rass, Emilie ; Germann, Susanne Manuela; Bertrand, Pascale ; Hickson, Ian David; Lopez, Bernard S. .

In: Cell Reports, Vol. 5, No. 1, 17.10.2013, p. 21-28.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Grabarz, A, Guirouilh-Barbat, J, Barascu, A, Pennarun, G, Genet, D, Rass, E, Germann, SM, Bertrand, P, Hickson, ID & Lopez, BS 2013, 'A Role for BLM in Double-Strand Break Repair Pathway Choice: Prevention of CtIP/Mre11-Mediated Alternative Nonhomologous End-Joining.', Cell Reports, vol. 5, no. 1, pp. 21-28. https://doi.org/10.1016/j.celrep.2013.08.034.

APA

Grabarz, A., Guirouilh-Barbat, J., Barascu, A., Pennarun, G., Genet, D., Rass, E., ... Lopez, B. S. (2013). A Role for BLM in Double-Strand Break Repair Pathway Choice: Prevention of CtIP/Mre11-Mediated Alternative Nonhomologous End-Joining. Cell Reports, 5(1), 21-28. https://doi.org/10.1016/j.celrep.2013.08.034.

Vancouver

Grabarz A, Guirouilh-Barbat J, Barascu A, Pennarun G, Genet D, Rass E et al. A Role for BLM in Double-Strand Break Repair Pathway Choice: Prevention of CtIP/Mre11-Mediated Alternative Nonhomologous End-Joining. Cell Reports. 2013 Oct 17;5(1):21-28. https://doi.org/10.1016/j.celrep.2013.08.034.

Author

Grabarz, Anastazja ; Guirouilh-Barbat, Josée ; Barascu, Aurelia ; Pennarun, Gaëlle ; Genet, Diane ; Rass, Emilie ; Germann, Susanne Manuela ; Bertrand, Pascale ; Hickson, Ian David ; Lopez, Bernard S. . / A Role for BLM in Double-Strand Break Repair Pathway Choice: Prevention of CtIP/Mre11-Mediated Alternative Nonhomologous End-Joining. In: Cell Reports. 2013 ; Vol. 5, No. 1. pp. 21-28.

Bibtex

@article{c98889a56d5f4e609ecb04dc31209241,
title = "A Role for BLM in Double-Strand Break Repair Pathway Choice: Prevention of CtIP/Mre11-Mediated Alternative Nonhomologous End-Joining.",
abstract = "The choice of the appropriate double-strand break (DSB) repair pathway isessential for the maintenance of genomic stability. Here, we show that the Bloom syndrome gene product, BLM, counteracts CtIP/MRE11-dependent long-range deletions(>200 bp) generated by alternative end-joining (A-EJ). BLM represses A-EJ in anepistatic manner with 53BP1 and RIF1 and is required forionizing-radiation-induced 53BP1 focus assembly. Conversely, in the absence of53BP1 or RIF1, BLM promotes formation of A-EJ long deletions, consistent with arole for BLM in DSB end resection. These data highlight a dual role for BLM that influences the DSB repair pathway choice: (1) protection against CtIP/MRE11long-range deletions associated with A-EJ and (2) promotion of DNA resection.These antagonist roles can be regulated, according to cell-cycle stage, byinteracting partners such as 53BP1 and TopIII, to avoid unscheduled resectionthat might jeopardize genome integrity.",
keywords = "The Faculty of Health and Medical Sciences, Center for Healthy Ageing",
author = "Anastazja Grabarz and Jos{\'e}e Guirouilh-Barbat and Aurelia Barascu and Ga{\"e}lle Pennarun and Diane Genet and Emilie Rass and Germann, {Susanne Manuela} and Pascale Bertrand and Hickson, {Ian David} and Lopez, {Bernard S.}",
year = "2013",
month = "10",
day = "17",
doi = "10.1016/j.celrep.2013.08.034.",
language = "English",
volume = "5",
pages = "21--28",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - A Role for BLM in Double-Strand Break Repair Pathway Choice: Prevention of CtIP/Mre11-Mediated Alternative Nonhomologous End-Joining.

AU - Grabarz, Anastazja

AU - Guirouilh-Barbat, Josée

AU - Barascu, Aurelia

AU - Pennarun, Gaëlle

AU - Genet, Diane

AU - Rass, Emilie

AU - Germann, Susanne Manuela

AU - Bertrand, Pascale

AU - Hickson, Ian David

AU - Lopez, Bernard S.

PY - 2013/10/17

Y1 - 2013/10/17

N2 - The choice of the appropriate double-strand break (DSB) repair pathway isessential for the maintenance of genomic stability. Here, we show that the Bloom syndrome gene product, BLM, counteracts CtIP/MRE11-dependent long-range deletions(>200 bp) generated by alternative end-joining (A-EJ). BLM represses A-EJ in anepistatic manner with 53BP1 and RIF1 and is required forionizing-radiation-induced 53BP1 focus assembly. Conversely, in the absence of53BP1 or RIF1, BLM promotes formation of A-EJ long deletions, consistent with arole for BLM in DSB end resection. These data highlight a dual role for BLM that influences the DSB repair pathway choice: (1) protection against CtIP/MRE11long-range deletions associated with A-EJ and (2) promotion of DNA resection.These antagonist roles can be regulated, according to cell-cycle stage, byinteracting partners such as 53BP1 and TopIII, to avoid unscheduled resectionthat might jeopardize genome integrity.

AB - The choice of the appropriate double-strand break (DSB) repair pathway isessential for the maintenance of genomic stability. Here, we show that the Bloom syndrome gene product, BLM, counteracts CtIP/MRE11-dependent long-range deletions(>200 bp) generated by alternative end-joining (A-EJ). BLM represses A-EJ in anepistatic manner with 53BP1 and RIF1 and is required forionizing-radiation-induced 53BP1 focus assembly. Conversely, in the absence of53BP1 or RIF1, BLM promotes formation of A-EJ long deletions, consistent with arole for BLM in DSB end resection. These data highlight a dual role for BLM that influences the DSB repair pathway choice: (1) protection against CtIP/MRE11long-range deletions associated with A-EJ and (2) promotion of DNA resection.These antagonist roles can be regulated, according to cell-cycle stage, byinteracting partners such as 53BP1 and TopIII, to avoid unscheduled resectionthat might jeopardize genome integrity.

KW - The Faculty of Health and Medical Sciences

KW - Center for Healthy Ageing

U2 - 10.1016/j.celrep.2013.08.034.

DO - 10.1016/j.celrep.2013.08.034.

M3 - Journal article

VL - 5

SP - 21

EP - 28

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 1

ER -

ID: 57286440