A third link connecting aging with double strand break repair

被引：19

作者：

Engels, William R. ^{[1
]}

Johnson-Schlitz, Dena ^{[1
]}

Flores, Carlos ^{[1
]}

White, Lisa ^{[1
]}

Preston, Christine R. ^{[1
]}

机构：

[1] Univ Wisconsin, Dept Genet, Madison, WI 53706 USA

来源：

CELL CYCLE | 2007年 / 6卷 / 02期

关键词：

aging; DNA repair; double-strand break; non homologous end-joining; single-strand annealing; homologous repair;

D O I：

10.4161/cc.6.2.3758

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Until recently, the connection between aging and DNA repair has rested on two classes of observation. First, DNA damage and unrepaired double-strand breaks (DSBs) accumulate with age. Second, several defects in DNA repair genes are associated with early onset of age-related diseases and other signs of premature aging. Now, a third link has emerged: The mechanisms by which cells repair DSB damage can change dramatically with age, shifting from simpler end-joining processes in younger organisms to homologous mechanisms in which missing genetic information is restored through use of a template. So far this third link between aging and DNA repair has only been observed in a small number of experimental systems, and cannot yet claim the generality of the other two. Here we review the evidence for this phenomenon and present new data testing models for the underlying causes. If the generality of age-related changes in DSB repair pathway usage can be established, it will provide a new insight into the underlying molecular basis of aging and how evolution has shaped these processes.

引用

页码：131 / 135

页数：5

共 42 条

[11] Hierarchical deterioration of body systems in Werner's syndrome: Implications for normal ageing [J].