Cheng Z F, Zuo Y, Li Z, Rudd K E, Deutscher M P
Department of Biochemistry and Molecular Biology, University of Miami School of Medicine, Miami, Florida 33101-6129, USA.
J Biol Chem. 1998 Jun 5;273(23):14077-80. doi: 10.1074/jbc.273.23.14077.
vacB, a gene previously shown to be required for expression of virulence in Shigella and enteroinvasive Escherichia coli, has been found to encode the 3'-5' exoribonuclease, RNase R. Thus, cloning of E. coli vacB led to overexpression of RNase R activity, and partial deletion or interruption of the cloned gene abolished this overexpression. Interruption of the chromosomal copy of vacB eliminated endogenous RNase R activity; however, the absence of RNase R by itself had no effect on cell growth. In contrast, cells lacking both RNase R and polynucleotide phosphorylase were found to be inviable. These data indicate that RNase R participates in an essential cell function in addition to its role in virulence. The identification of the vacB gene product as RNase R should aid in understanding how the virulence phenotype in enterobacteria is expressed and regulated. On the basis of this information we propose that vacB be renamed rnr.
vacB基因先前已被证明是志贺氏菌和肠侵袭性大肠杆菌中表达毒力所必需的,现已发现它编码3'-5'外切核糖核酸酶RNase R。因此,大肠杆菌vacB基因的克隆导致RNase R活性的过表达,而克隆基因的部分缺失或中断消除了这种过表达。vacB染色体拷贝的中断消除了内源性RNase R活性;然而,单独缺失RNase R对细胞生长没有影响。相比之下,同时缺乏RNase R和多核苷酸磷酸化酶的细胞被发现无法存活。这些数据表明,RNase R除了在毒力中发挥作用外,还参与一种基本的细胞功能。将vacB基因产物鉴定为RNase R应有助于理解肠道细菌中毒力表型是如何表达和调控的。基于这些信息,我们建议将vacB重新命名为rnr。