How Cells Respond to DNA Breaks in Mitosis

被引：47

作者：

Blackford, Andrew N. ^{[1
,2
]}

Stucki, Manuel ^{[3
]}

机构：

[1] Univ Oxford, John Radcliffe Hosp, MRC Weatherall Inst Mol Med, Dept Oncol, Oxford OX3 9DS, England

[2] Univ Oxford, Canc Res UK, MRC Oxford Inst Radiat Oncol, Oxford OX3 7DQ, England

[3] Univ Zurich, Dept Gynecol, Wagistr 14, CH-8952 Schlieren, Switzerland

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 2020年 / 45卷 / 04期

关键词：

DOUBLE-STRAND BREAKS; DAMAGE-RESPONSE; STRUCTURAL BASIS; TELOMERES JOIN; PROTEIN-KINASE; FRAGILE SITES; CHECKPOINT; REPAIR; 53BP1; ACTIVATION;

D O I：

10.1016/j.tibs.2019.12.010

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

DNA double-strand breaks (DSBs) are highly toxic lesions that can lead to chromosomal instability if they are not repaired correctly. DSBs are especially dangerous in mitosis when cells go through the complex process of equal chromosome segregation into daughter cells. When cells encounter DSBs in interphase, they are able to arrest the cell cycle until the breaks are repaired before entering mitosis. However, when DSBs occur during mitosis, cells no longer arrest but prioritize completion of cell division over repair of DNA damage. This review focuses on recent progress in our understanding of the mechanisms that allow mitotic cells to postpone DSB repair without accumulating massive chromosomal instability. Additionally, we review possible physiological consequences of failed DSB responses in mitosis.

引用

页码：321 / 331

页数：11

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