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RAD52可防止人类细胞中受干扰的复制叉处依赖于的复制缺口的积累。 （你提供的原文中“-dependent”这里“-”部分缺失关键信息，可能影响准确理解，但按要求照译了）

RAD52 prevents accumulation of -dependent replication gaps at perturbed replication forks in human cells.

作者信息

Di Biagi Ludovica, Marozzi Giorgia, Malacaria Eva, Honda Masayoshi, Aiello Francesca Antonella, Valenzisi Pasquale, Spies Maria, Franchitto Annapaola, Pichierri Pietro

机构信息

Mechanisms, Biomarkers and Models Section, Genome Stability Group, Department of Environment and Health, Istituto Superiore di Sanità - Viale Regina Elena 299, 00161 Rome (Italy).

Department of Biochemistry and Molecular Biology, University of Iowa Carver College of Medicine, 51 Newton Road, Iowa City, IA 52242 (USA).

出版信息

bioRxiv. 2024 Aug 17:2023.04.12.536536. doi: 10.1101/2023.04.12.536536.

DOI:10.1101/2023.04.12.536536
PMID:37090680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10120653/
Abstract

Replication gaps can arise as a consequence of perturbed DNA replication and their accumulation might undermine the stability of the genome. Loss of RAD52, a protein involved in the regulation of fork reversal, promotes accumulation of parental ssDNA gaps during replication perturbation. Here, we demonstrate that this is due to the engagement of downstream of the extensive degradation of perturbed replication forks after their reversal, and is not dependent on PrimPol. is hyper-recruited at parental ssDNA in the absence of RAD52, and this recruitment is dependent on fork reversal enzymes and RAD51. Of note, we report that the interaction between and RAD51 is stimulated by RAD52 inhibition, and -dependent gap accumulation requires nucleation of RAD51 suggesting that it occurs downstream strand invasion. Altogether, our data indicate that RAD51- -dependent repriming is essential to promote fork restart and limit DNA damage accumulation when RAD52 function is disabled.

摘要

复制缺口可能因DNA复制受到干扰而出现，其积累可能会破坏基因组的稳定性。参与叉逆转调控的蛋白质RAD52的缺失会促进复制干扰期间亲本单链DNA缺口的积累。在这里，我们证明这是由于叉逆转后受干扰的复制叉广泛降解的下游的参与，并且不依赖于PrimPol。在没有RAD52的情况下， 在亲本单链DNA上被过度招募，并且这种招募依赖于叉逆转酶和RAD51。值得注意的是，我们报告说RAD52抑制会刺激 与RAD51之间的相互作用，并且依赖于 的缺口积累需要RAD51的成核，这表明它发生在下游链入侵之后。总之，我们的数据表明，当RAD52功能被禁用时，依赖于RAD51- 的重新引发对于促进叉重新启动和限制DNA损伤积累至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/b1948c539d27/nihpp-2023.04.12.536536v2-f0011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/1c4a703f691b/nihpp-2023.04.12.536536v2-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/6ca792b9def9/nihpp-2023.04.12.536536v2-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/b8a043051719/nihpp-2023.04.12.536536v2-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/bfe5783dde6c/nihpp-2023.04.12.536536v2-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/12d91ca95618/nihpp-2023.04.12.536536v2-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/fb55dfb7788c/nihpp-2023.04.12.536536v2-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/eae37ab297f2/nihpp-2023.04.12.536536v2-f0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/b1948c539d27/nihpp-2023.04.12.536536v2-f0011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/1c4a703f691b/nihpp-2023.04.12.536536v2-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/6ca792b9def9/nihpp-2023.04.12.536536v2-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/b8a043051719/nihpp-2023.04.12.536536v2-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/bfe5783dde6c/nihpp-2023.04.12.536536v2-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/12d91ca95618/nihpp-2023.04.12.536536v2-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/fb55dfb7788c/nihpp-2023.04.12.536536v2-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/eae37ab297f2/nihpp-2023.04.12.536536v2-f0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25f4/11423105/b1948c539d27/nihpp-2023.04.12.536536v2-f0011.jpg

相似文献

[1]
RAD52 prevents accumulation of -dependent replication gaps at perturbed replication forks in human cells.

bioRxiv. 2024-8-17

[2]
Rad52 prevents excessive replication fork reversal and protects from nascent strand degradation.

Nat Commun. 2019-3-29

[3]
CHK1 phosphorylates PRIMPOL to promote replication stress tolerance.

Sci Adv. 2022-4

[4]
A double-ring of human RAD52 remodels replication forks restricting fork reversal.

bioRxiv. 2024-9-18

[5]
PRIMPOL-Mediated Adaptive Response Suppresses Replication Fork Reversal in BRCA-Deficient Cells.

Mol Cell. 2019-10-29

[6]
WRNIP1 protects stalled forks from degradation and promotes fork restart after replication stress.

EMBO J. 2016-7-1

[7]
Smarcal1-Mediated Fork Reversal Triggers Mre11-Dependent Degradation of Nascent DNA in the Absence of Brca2 and Stable Rad51 Nucleofilaments.

Mol Cell. 2017-9-7

[8]
CRISPR knockout genome-wide screens identify the HELQ-RAD52 axis in regulating the repair of cisplatin-induced single stranded DNA gaps.

bioRxiv. 2024-4-20

[9]
Fork Cleavage-Religation Cycle and Active Transcription Mediate Replication Restart after Fork Stalling at Co-transcriptional R-Loops.

Mol Cell. 2019-11-20

[10]
Distinct RAD51 associations with RAD52 and BCCIP in response to DNA damage and replication stress.

Cancer Res. 2008-4-15

引用本文的文献

[1]
RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis.

PLoS Genet. 2024-11-19

本文引用的文献

[1]
Phosphorylation status of MUS81 is a modifier of Olaparib sensitivity in BRCA2-deficient cells.

Nucleic Acids Res. 2023-7-21

[2]
POLQ seals post-replicative ssDNA gaps to maintain genome stability in BRCA-deficient cancer cells.

Mol Cell. 2022-12-15

[3]
POLθ prevents MRE11-NBS1-CtIP-dependent fork breakage in the absence of BRCA2/RAD51 by filling lagging-strand gaps.

Mol Cell. 2022-11-17

[4]
Emetine blocks DNA replication via proteosynthesis inhibition not by targeting Okazaki fragments.

Life Sci Alliance. 2022-9-9

[5]
Structures of the human CST-Polα-primase complex bound to telomere templates.

Nature. 2022-8

[6]
Exploiting replication gaps for cancer therapy.

Mol Cell. 2022-7-7

[7]
Replication Protein A Phosphorylation Facilitates RAD52-Dependent Homologous Recombination in BRCA-Deficient Cells.

Mol Cell Biol. 2022-2-17

[8]
BRCA2 associates with MCM10 to suppress PRIMPOL-mediated repriming and single-stranded gap formation after DNA damage.

Nat Commun. 2021-10-13

[9]
Temporally distinct post-replicative repair mechanisms fill PRIMPOL-dependent ssDNA gaps in human cells.

Mol Cell. 2021-10-7

[10]
Replication gaps are a key determinant of PARP inhibitor synthetic lethality with BRCA deficiency.

Mol Cell. 2021-8-5

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