Break-induced replication and recombinational telomere elongation in yeast

被引:263
作者
McEachern, Michael J. [1 ]
Haber, James E.
机构
[1] Univ Georgia, Dept Genet, Athens, GA 30602 USA
[2] Brandeis Univ, Dept Biol, Waltham, MA 02454 USA
[3] Brandeis Univ, Rosensteil Ctr, Waltham, MA 02454 USA
关键词
homologous recombination; yeast; double-strand break repair;
D O I
10.1146/annurev.biochem.74.082803.133234
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
When a telomere becomes unprotected or if only one end of a chromosomal double-strand break succeeds in recombining with a template sequence, DNA can be repaired by a recombination-dependent DNA replication process termed break-induced replication (BIR). In budding yeasts, there are two BIR pathways, one dependent on the Rad51 recombinase protein and one Rad51 independent; these two repair processes lead to different types of survivors in cells lacking the telomerasc enzyme that is required for normal telomere maintenance. Recombination at telomeres is triggered by either execssive telomere shortening or disruptions in the function of telomere-binding proteins. Telomere elongation by BIR appears to often occur through a "roll and spread" mechanism. In this process, a telomeric circle produced by recombination at a dysfunctional telomere acts as a template for a rolling circle BIR event to form an elongated telomere. Additional BIR events can then copy the elongated sequence to all other telomeres.
引用
收藏
页码:111 / 135
页数:25
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