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突变偏向性表明复制终止发生在dif位点附近,而非Ter位点处。

Mutational bias suggests that replication termination occurs near the dif site, not at Ter sites.

作者信息

Hendrickson Heather, Lawrence Jeffrey G

机构信息

Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA 15260, USA.

出版信息

Mol Microbiol. 2007 Apr;64(1):42-56. doi: 10.1111/j.1365-2958.2007.05596.x.

DOI:10.1111/j.1365-2958.2007.05596.x
PMID:17376071
Abstract

In bacteria, Ter sites bound to Tus/Rtp proteins halt replication forks moving only in one direction, providing a convenient mechanism to terminate them once the chromosome had been replicated. Considering the importance of replication termination and its position as a checkpoint in cell division, the accumulated knowledge on these systems has not dispelled fundamental questions regarding its role in cell biology: why are there so many copies of Ter, why are they distributed over such a large portion of the chromosome, why is the tus gene not conserved among bacteria, and why do tus mutants lack measurable phenotypes? Here we examine bacterial genomes using bioinformatics techniques to identify the region(s) where DNA polymerase III-mediated replication has historically been terminated. We find that in both Escherichia coli and Bacillus subtilis, changes in mutational bias patterns indicate that replication termination most likely occurs at or near the dif site. More importantly, there is no evidence from mutational bias signatures that replication forks originating at oriC have terminated at Ter sites. We propose that Ter sites participate in halting replication forks originating from DNA repair events, and not those originating at the chromosomal origin of replication.

摘要

在细菌中,与Tus/Rtp蛋白结合的Ter位点仅阻止复制叉沿一个方向移动,为染色体复制完成后终止复制叉提供了一种简便机制。考虑到复制终止的重要性及其作为细胞分裂检查点的地位,关于这些系统积累的知识并未消除有关其在细胞生物学中作用的基本问题:为什么有这么多Ter拷贝,为什么它们分布在染色体的如此大的部分上,为什么tus基因在细菌中不保守,以及为什么tus突变体缺乏可测量的表型?在这里,我们使用生物信息学技术检查细菌基因组,以识别历史上DNA聚合酶III介导的复制终止的区域。我们发现,在大肠杆菌和枯草芽孢杆菌中,突变偏向模式的变化表明复制终止最有可能发生在dif位点或其附近。更重要的是,从突变偏向特征中没有证据表明源自oriC的复制叉在Ter位点终止。我们提出,Ter位点参与阻止源自DNA修复事件的复制叉,而不是源自染色体复制起点的复制叉。

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