Chromatin remodeling and spatial concerns in DNA double-strand break repair

被引：4

作者：

Downs, Jessica A. ^{[1
]}

Gasser, Susan M. ^{[2
,3
]}

机构：

[1] Inst Canc Res, Epigenet & Genome Stabil Team, 237 Fulham Rd, London SW3 6JB, England

[2] ISREC Fdn, Rue Bugnon 25a, CH-1005 Lausanne, Switzerland

[3] Univ Lausanne, Agora Canc Res Ctr, Rue Bugnon 25a, CH-1005 Lausanne, Switzerland

来源：

CURRENT OPINION IN CELL BIOLOGY | 2024年 / 90卷

基金：

瑞士国家科学基金会;

关键词：

HOMOLOGOUS RECOMBINATION; DAMAGE RESPONSE; END RESECTION; TRANSCRIPTION; MECHANISMS; DYNAMICS; REVEALS; GENOME; HETEROCHROMATIN; RECRUITMENT;

D O I：

10.1016/j.ceb.2024.102405

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The substrate for the repair of DNA damage in living cells is not DNA but chromatin. Chromatin bears a range of modifications, which in turn bind ligands that compact or open chromatin structure, and determine its spatial organization within the nucleus. In some cases, RNA in the form of RNA:DNA hybrids or R-loops modulates DNA accessibility. Each of these parameters can favor particular pathways of repair. Chromatin or nucleosome remodelers are key regulators of chromatin structure, and a number of remodeling complexes are implicated in DNA repair. We cover novel insights into the impact of chromatin structure, nuclear organization, R-loop formation, nuclear actin, and nucleosome remodelers in DNA double- strand break repair, focusing on factors that alter repair functional upon ablation.

引用

页数：10

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