...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Translesion DNA polymerases are required for spontaneous deletion formation in Salmonella typhimurium
【24h】

Translesion DNA polymerases are required for spontaneous deletion formation in Salmonella typhimurium

机译：鼠伤寒沙门氏菌自发缺失形成需要跨病变DNA聚合酶

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

How spontaneous deletions form in bacteria is still a partly unresolved problem. Here, we show that deletion formation in Salmonella typhimurium requires the presence of functional translesion polymerases. First, in wild-type bacteria, removal of the known translesion DNA polymerases, Polll (polB), PollV (dinB), PolV (umuDC), and SamAB (samAB), resulted in a 10-fold decrease in the deletion rate, indicating that 90% of all spontaneous deletions require these polymerates for their formation. Second, overex-pression of these polymerases by derepression of the DNA dam-age-inducible LexA regulon caused a 25-fold increase in deletion rate that depended on the presence of functional translesion polymerases. Third, overexpression of the polymerases Polll and PollV from a plasmid increased the deletion rate 12- to 30-fold, respectively. Last, in a recBC~- mutant where dsDNA ends are stabilized due to the lack of the end-processing nuclease RecBC, the deletion rate was increased 20-fold. This increase depended on the translesion polymerases. In lexA(def) mutant cells with constitutive SOS expression, a 10-fold increase in DNA breaks was observed. Inactivation of all 4 translesion polymerases in the lexA(def) mutant reduced the deletion rate 250-fold without any concomitant reduction in the amount of DNA breaks. Mutational inactivation of 3 endonucleases under LexA control reduced the number of DNA breaks to the wild-type level in a lexA(def) mutant with a concomitant 50-fold reduction in deletion rate. These findings suggest that the translesion polymerases are not involved in forming the DNA breaks, but that they require them to stimulate deletion formation.
机译：细菌中自发缺失的形成方式仍是部分尚未解决的问题。在这里，我们显示鼠伤寒沙门氏菌中的删除形成需要功能性转移聚合酶的存在。首先，在野生型细菌中，去除已知的病灶DNA聚合酶Polll（polB），PollV（dinB），PolV（umuDC）和SamAB（samAB），导致删除率降低了10倍，表明90％的自发缺失需要这些聚合体才能形成。其次，通过抑制DNA损伤诱导型LexA调节子来过度表达这些聚合酶，导致缺失率增加25倍，这取决于功能性病变聚合酶的存在。第三，从质粒中过表达聚合酶Polll和PollV分别使缺失率增加了12至30倍。最后，在由于末端加工核酸酶RecBC的缺乏而使dsDNA末端稳定的recBC-突变体中，缺失率增加了20倍。这种增加取决于跨病变的聚合酶。在具有组成性SOS表达的lexA（def）突变细胞中，观察到DNA断裂增加了10倍。失活lexA（def）突变体中的所有4种跨病变聚合酶，可将删除率降低250倍，而DNA断裂量不会随之减少。在LexA控制下3种核酸内切酶的突变失活将lexA（def）突变体中的DNA断裂数减少到野生型水平，同时缺失率降低了50倍。这些发现表明，跨病变的聚合酶不参与DNA断裂的形成，但要求它们刺激缺失的形成。

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