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DNA double strand break repair in Escherichia coli?perturbs cell division and chromosome dynamics

机译:DNA双链缓解修复<斜体>大肠杆菌?Perturbs细胞分裂和染色体动力学

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To prevent the transmission of damaged genomic material between generations, cells require a system for accommodating DNA repair within their cell cycles. We have previously shown that Escherichia coli cells subject to a single, repairable site-specific DNA double-strand break (DSB) per DNA replication cycle reach a new average cell length, with a negligible effect on population growth rate. We show here that this new cell size distribution is caused by a DSB repair-dependent delay in completion of cell division. This delay occurs despite unperturbed cell size regulated initiation of both chromosomal DNA replication and cell division. Furthermore, despite DSB repair altering the profile of DNA replication across the genome, the time required to complete chromosomal duplication is invariant. The delay in completion of cell division is accompanied by a DSB repair-dependent delay in individualization of sister nucleoids. We suggest that DSB repair events create inter-sister connections that persist until those chromosomes are separated by a closing septum.
机译:为了防止世代之间的损坏基因组材料的传播,细胞需要一种用于在其细胞周期内容纳DNA修复的系统。我们之前已经表明,每个DNA复制循环受到单一,可修复的位点特异性DNA双链断裂(DSB)的大肠杆菌细胞达到新的平均细胞长度,对人群生长率的影响可忽略不计。我们在这里展示了这种新的细胞大小分布是由Cell划分完成完成的DSB修复依赖延迟引起的。尽管染色体DNA复制和细胞分裂的染色体大小调节启动,但这种延迟也会发生。此外,尽管DSB修复在基因组中改变DNA复制的谱,但完全染色体重复所需的时间是不变的。细胞分裂完成的延迟伴随着DSB修复依赖性延迟,患者核毒儿的个体化。我们建议DSB修复事件创建持续存在的妹妹连接,直到这些染色体通过闭合隔膜分开。

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