...
首页> 外文期刊>Journal of Molecular Biology >EFFECTS ON MRNA DEGRADATION BY ESCHERICHIA COLI TRANSCRIPTION TERMINATION FACTOR RHO AND PBR322 COPY NUMBER CONTROL PROTEIN ROP
【24h】

EFFECTS ON MRNA DEGRADATION BY ESCHERICHIA COLI TRANSCRIPTION TERMINATION FACTOR RHO AND PBR322 COPY NUMBER CONTROL PROTEIN ROP

机译:大肠埃希氏菌转录终止因子Rho和PBR322拷贝数控制蛋白对MRNA降解的影响

获取原文
获取原文并翻译 | 示例

摘要

Mutants in Escherichia coli transcription termination factor Rho, termed rho(nusD), were previously isolated based on their ability to block the growth of bacteriophage T4. Here we show that rho(nusD) strains have decreased average half-lives for bulk cellular mRNA. Decreased E. coli message lifetimes could be because of increased ribonuclease activity in the rho mutant cells: if a Rho-dependent terminator precedes a ribonuclease gene, weaker termination in the rho mutants could lead to nuclease overexpression. However, inactivation of ribonuclease genes in rho026 cells did not relieve the defective phage growth. Unexpectedly, expression of the pBR322 Rop protein, a structure-specific, sequence-independent RNA-binding protein, in rho(nusD) cells restored the ability of T4 to grow and prolonged cellular message half-life in both the wild-type and the rho026 mutant. These results suggest that it is the RNA-binding ability of Rho rather than its transcription termination function that is important for the inhibition of bacteriophage growth and the shorter bulk mRNA lifetime. We propose that altered interaction of the mutant Rho with mRNA could make the RNA more susceptible to degradation. The inability of the RNA-binding proteins SrmB and DeaD to reverse the who mutant phenotype when each is overexpressed implies that the required RNA interactions are specific. The results show novel roles for Rho and Rop in mRNA stability. (C) 1997 Academic Press Limited. [References: 79]
机译:大肠杆菌转录终止因子Rho中的突变体称为rho(nusD),先前已根据其阻断噬菌体T4生长的能力进行了分离。在这里,我们显示rho(nusD)菌株具有降低的大量细胞mRNA的平均半衰期。大肠杆菌信息寿命的缩短可能是由于rho突变细胞中核糖核酸酶活性的增加:如果Rho依赖性终止子先于核糖核酸酶基因,则rho突变体中较弱的终止可能导致核酸酶过表达。但是,rho026细胞中核糖核酸酶基因的失活并不能缓解有缺陷的噬菌体的生长。出乎意料的是,rho(nusD)细胞中pBR322 Rop蛋白(一种结构特异性,不依赖序列的RNA结合蛋白)的表达恢复了T4在野生型和野生型中生长和延长细胞信息半衰期的能力。 rho026突变体。这些结果表明,Rho的RNA结合能力而不是其转录终止功能对抑制噬菌体生长和缩短整体mRNA寿命很重要。我们提出,突变体Rho与mRNA相互作用的改变可使RNA更易于降解。当每种过表达时,RNA结合蛋白SrmB和DeaD无法逆转谁的突变体表型,这意味着所需的RNA相互作用是特异性的。结果显示Rho和Rop在mRNA稳定性中的新作用。 (C)1997 Academic Press Limited。 [参考:79]

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