...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Scientific reports. >Large XPF-dependent deletions following misrepair of a DNA double strand break are prevented by the RNA:DNA helicase Senataxin
【24h】

Large XPF-dependent deletions following misrepair of a DNA double strand break are prevented by the RNA:DNA helicase Senataxin

机译：通过RNA预防DNA双链突破的误区后依赖于大的XPF依赖性缺失：DNA Helicase Senataxin

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Deletions and chromosome re-arrangements are common features of cancer cells. We have established a new two-component system reporting on epigenetic silencing or deletion of an actively transcribed gene adjacent to a double-strand break (DSB). Unexpectedly, we find that a targeted DSB results in a minority (10%) misrepair event of kilobase deletions encompassing the DSB site and transcribed gene. Deletions are reduced upon RNaseH1 over-expression and increased after knockdown of the DNA:RNA helicase Senataxin, implicating a role for DNA:RNA hybrids. We further demonstrate that the majority of these large deletions are dependent on the 3′ flap endonuclease XPF. DNA:RNA hybrids were detected by DNA:RNA immunoprecipitation in our system after DSB generation. These hybrids were reduced by RNaseH1 over-expression and increased by Senataxin knock-down, consistent with a role in deletions. Overall, these data are consistent with DNA:RNA hybrid generation at the site of a DSB, mis-processing of which results in genome instability in the form of large deletions.
机译：缺失和染色体重新安排是癌细胞的常见特征。我们已经建立了关于表观遗传沉默或缺失与双链断裂（DSB）相邻的主动转录基因的新的双组分系统报告。出乎意料的是，我们发现目标DSB导致少数群体（<10％）千碱基缺失的误解事件，包括DSB网站和转录基因。在RNASEH1过表达上减少缺失并在DNA敲低后增加：RNA Helicase Senataxin，暗示DNA：RNA杂种的作用。我们进一步证明，这些大缺失的大部分依赖于3'襟翼内切核酸酶XPF。 DNA：通过DNA检测到RNA杂交物：在DSB生成后我们的系统中的RNA免疫沉淀。通过RNASEH1过表达减少这些杂种并通过Senataxin敲低增加，与缺失中的作用一致。总的来说，这些数据与DNA：RNA杂交生成在DSB的位点，其误解过程导致基因组不稳定性以大缺失的形式。

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