RAD52 Facilitates Mitotic DNA Synthesis Following Replication Stress

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

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RAD52 Facilitates Mitotic DNA Synthesis Following Replication Stress. / Bhowmick, Rahul; Minocherhomji, Sheroy; Hickson, Ian D.

In: Molecular Cell, Vol. 64, No. 6, 15.12.2016, p. 1117-1126.

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

Harvard

Bhowmick, R, Minocherhomji, S & Hickson, ID 2016, 'RAD52 Facilitates Mitotic DNA Synthesis Following Replication Stress', Molecular Cell, vol. 64, no. 6, pp. 1117-1126. https://doi.org/10.1016/j.molcel.2016.10.037

APA

Bhowmick, R., Minocherhomji, S., & Hickson, I. D. (2016). RAD52 Facilitates Mitotic DNA Synthesis Following Replication Stress. Molecular Cell, 64(6), 1117-1126. https://doi.org/10.1016/j.molcel.2016.10.037

Vancouver

Bhowmick R, Minocherhomji S, Hickson ID. RAD52 Facilitates Mitotic DNA Synthesis Following Replication Stress. Molecular Cell. 2016 Dec 15;64(6):1117-1126. https://doi.org/10.1016/j.molcel.2016.10.037

Author

Bhowmick, Rahul ; Minocherhomji, Sheroy ; Hickson, Ian D. / RAD52 Facilitates Mitotic DNA Synthesis Following Replication Stress. In: Molecular Cell. 2016 ; Vol. 64, No. 6. pp. 1117-1126.

Bibtex

@article{a42cc91b95714e50972126dbb183ec9f,
title = "RAD52 Facilitates Mitotic DNA Synthesis Following Replication Stress",
abstract = "Homologous recombination (HR) is necessary to counteract DNA replication stress. Common fragile site (CFS) loci are particularly sensitive to replication stress and undergo pathological rearrangements in tumors. At these loci, replication stress frequently activates DNA repair synthesis in mitosis. This mitotic DNA synthesis, termed MiDAS, requires the MUS81-EME1 endonuclease and a non-catalytic subunit of the Pol-delta complex, POLD3. Here, we examine the contribution of HR factors in promoting MiDAS in human cells. We report that RAD51 and BRCA2 are dispensable for MiDAS but are required to counteract replication stress at CFS loci during S-phase. In contrast, MiDAS is RAD52 dependent, and RAD52 is required for the timely recruitment of MUS81 and POLD3 to CFSs in early mitosis. Our results provide further mechanistic insight into MiDAS and define a specific function for human RAD52. Furthermore, selective inhibition of MiDAS may comprise a potential therapeutic strategy to sensitize cancer cells undergoing replicative stress.",
author = "Rahul Bhowmick and Sheroy Minocherhomji and Hickson, {Ian D}",
note = "Copyright {\textcopyright} 2016 Elsevier Inc. All rights reserved.",
year = "2016",
month = dec,
day = "15",
doi = "10.1016/j.molcel.2016.10.037",
language = "English",
volume = "64",
pages = "1117--1126",
journal = "Molecular Cell",
issn = "1097-2765",
publisher = "Cell Press",
number = "6",

}

RIS

TY - JOUR

T1 - RAD52 Facilitates Mitotic DNA Synthesis Following Replication Stress

AU - Bhowmick, Rahul

AU - Minocherhomji, Sheroy

AU - Hickson, Ian D

N1 - Copyright © 2016 Elsevier Inc. All rights reserved.

PY - 2016/12/15

Y1 - 2016/12/15

N2 - Homologous recombination (HR) is necessary to counteract DNA replication stress. Common fragile site (CFS) loci are particularly sensitive to replication stress and undergo pathological rearrangements in tumors. At these loci, replication stress frequently activates DNA repair synthesis in mitosis. This mitotic DNA synthesis, termed MiDAS, requires the MUS81-EME1 endonuclease and a non-catalytic subunit of the Pol-delta complex, POLD3. Here, we examine the contribution of HR factors in promoting MiDAS in human cells. We report that RAD51 and BRCA2 are dispensable for MiDAS but are required to counteract replication stress at CFS loci during S-phase. In contrast, MiDAS is RAD52 dependent, and RAD52 is required for the timely recruitment of MUS81 and POLD3 to CFSs in early mitosis. Our results provide further mechanistic insight into MiDAS and define a specific function for human RAD52. Furthermore, selective inhibition of MiDAS may comprise a potential therapeutic strategy to sensitize cancer cells undergoing replicative stress.

AB - Homologous recombination (HR) is necessary to counteract DNA replication stress. Common fragile site (CFS) loci are particularly sensitive to replication stress and undergo pathological rearrangements in tumors. At these loci, replication stress frequently activates DNA repair synthesis in mitosis. This mitotic DNA synthesis, termed MiDAS, requires the MUS81-EME1 endonuclease and a non-catalytic subunit of the Pol-delta complex, POLD3. Here, we examine the contribution of HR factors in promoting MiDAS in human cells. We report that RAD51 and BRCA2 are dispensable for MiDAS but are required to counteract replication stress at CFS loci during S-phase. In contrast, MiDAS is RAD52 dependent, and RAD52 is required for the timely recruitment of MUS81 and POLD3 to CFSs in early mitosis. Our results provide further mechanistic insight into MiDAS and define a specific function for human RAD52. Furthermore, selective inhibition of MiDAS may comprise a potential therapeutic strategy to sensitize cancer cells undergoing replicative stress.

U2 - 10.1016/j.molcel.2016.10.037

DO - 10.1016/j.molcel.2016.10.037

M3 - Journal article

C2 - 27984745

VL - 64

SP - 1117

EP - 1126

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

IS - 6

ER -

ID: 172058782