Yeast Rad5 protein required for postreplication repair has a DNA helicase activity specific for replication fork regression.

Yeast Rad5 protein required for postreplication repair has a DNA helicase activity specific for replication fork regression.
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DOI:
10.1016/j.molcel.2007.07.030
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发表时间:
2007-10-12
期刊:
影响因子:
16
通讯作者:
Haracska L
Haracska L
中科院分区:
生物学1区
文献类型:
--
作者:
Blastyák A;Pintér L;Unk I;Prakash L;Prakash S;Haracska L

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模板DNA链中的损伤阻断复制叉的进展。在酿酒酵母中,通过DNA损伤的复制是由不同的Rad 6-Rad 18依赖性手段介导的,这些手段包括translesion合成和Rad 5依赖性复制后修复途径,该途径修复从受损模板合成的DNA中形成的不连续性。虽然translesion合成的特点,很少有人知道的机制,调节Rad 5依赖postreplicational修复。在这里,我们表明,酵母Rad 5具有DNA解旋酶活性,是专门为复制叉回归。在模型复制叉结构上,Rad 5协调地解开和退火新生链和亲本链,而不暴露延伸的单链区域。这些观察结果提供了深入了解postreplicational修复的机制,其中Rad 5行动促进模板转换为无错误的损伤旁路。
Lesions in the template DNA strand block the progression of the replication fork. In the yeast Saccharomyces cerevisiae, replication through DNA lesions is mediated by different Rad6-Rad18-dependent means, which include translesion synthesis and a Rad5-dependent postreplicational repair pathway that repairs the discontinuities that form in the DNA synthesized from damaged templates. Although translesion synthesis is well characterized, little is known about the mechanisms that modulate Rad5-dependent postreplicational repair. Here we show that yeast Rad5 has a DNA helicase activity that is specialized for replication fork regression. On model replication fork structures, Rad5 concertedly unwinds and anneals the nascent and the parental strands without exposing extended single-stranded regions. These observations provide insight into the mechanism of postreplicational repair in which Rad5 action promotes template switching for error-free damage bypass.
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