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酵母中的断裂诱导复制与重组性端粒延长

Break-induced replication and recombinational telomere elongation in yeast.

作者信息

McEachern Michael J, Haber James E

机构信息

Department of Genetics, University of Georgia, Athens, Georgia 30602, USA.

出版信息

Annu Rev Biochem. 2006;75:111-35. doi: 10.1146/annurev.biochem.74.082803.133234.

Abstract

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 telomerase enzyme that is required for normal telomere maintenance. Recombination at telomeres is triggered by either excessive 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.

摘要

当端粒变得无保护时,或者如果染色体双链断裂的只有一端成功与模板序列重组,DNA可以通过一种称为断裂诱导复制(BIR)的依赖重组的DNA复制过程进行修复。在芽殖酵母中,有两条BIR途径,一条依赖于Rad51重组酶蛋白,另一条不依赖Rad51;这两种修复过程在缺乏正常端粒维持所需的端粒酶的细胞中会导致不同类型的存活细胞。端粒处的重组由端粒过度缩短或端粒结合蛋白功能破坏引发。BIR介导的端粒延长似乎常常通过“滚动与扩展”机制发生。在此过程中,功能失调的端粒处重组产生的端粒环作为滚环BIR事件的模板,形成延长的端粒。随后的其他BIR事件可以将延长的序列复制到所有其他端粒。

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