...
【24h】

Transcription termination maintains chromosome integrity

机译:转录终止可维持染色体完整性

获取原文
获取原文并翻译 | 示例
           

摘要

DNA replication fork movement is impeded by collisions with transcription elongation complexes (TEC). We propose that a critical function of transcription termination factors is to prevent TEC from blocking DNA replication and inducing replication fork arrest, one consequence of which is DNA double-strand breaks. We show that inhibition of Rho-dependent transcription termination by bicyclo-mycin in Escherichia coli induced double-strand breaks. Cells deleted for Rho-cofactors nusA and nusG were hypersensitive to bicyclomycin, and had extensive chromosome fragmentation even in the absence of the drug. An RNA polymerase mutation that destabilizes TEC (rpoB*35) increased bicyclomycin resistance >40-fold. Double-strand break formation depended on DNA replication, and can be explained by replication fork collapse. Deleting recombination genes required for replication fork repair (recB and ruvC) increased sensitivity to bicyclomycin, as did loss of the replication fork reloading helicases rep and priA. We propose that Rho responds to a translocating replisome by releasing obstructing TEC.
机译:与转录延伸复合物(TEC)的碰撞阻碍了DNA复制叉的运动。我们提出转录终止因子的关键功能是防止TEC阻止DNA复制并诱导复制叉停滞,其结果之一就是DNA双链断裂。我们表明双环霉素在大肠杆菌中抑制Rho依赖的转录终止诱导双链断裂。缺失Rho辅助因子nusA和nusG的细胞对双环霉素非常敏感,即使在没有药物的情况下也具有广泛的染色体断裂。使TEC不稳定的RNA聚合酶突变(rpoB * 35)使双环霉素抗性增加> 40倍。双链断裂的形成取决于DNA的复制,可以用复制叉的崩溃来解释。删除复制叉修复所需的重组基因(recB和ruvC)会增加对双环霉素的敏感性,复制叉重新加载解旋酶rep和priA的缺失也会增加。我们建议Rho通过释放阻碍TEC来响应易位复制体。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号