Hase Yoichi, Yokoyama Shinichiro, Muto Akira, Himeno Hyouta
Department of Biochemistry and Molecular Biology, Faculty of Agriculture and Life Science, Hirosaki University, Hirosaki 036-8561, Japan.
RNA. 2009 Sep;15(9):1766-74. doi: 10.1261/rna.1687309. Epub 2009 Jul 20.
RsgA is a unique GTP hydrolytic protein in which GTPase activity is significantly enhanced by the small ribosomal subunit. Deletion of RsgA causes slow cell growth as well as defects in subunit assembly of the ribosome and 16S rRNA processing, suggesting its involvement in maturation of the small subunit. In this study, we found that removal of RsgA or inactivation of its ribosome small subunit-dependent GTPase activity provides Escherichia coli cells with resistance to high salt stress. Salt stress suppressed the defects in subunit assembly of the ribosome and processing of 16S rRNA as well as truncation of the 3' end of 16S rRNA in RsgA-deletion cells. In contrast, salt stress transiently impaired subunit assembly of the ribosome and processing of 16S rRNA and induced 3' truncation of 16S rRNA in wild-type cells. These results suggest that the action of RsgA on the ribosome, which usually facilitates maturation of the small subunit, disturbs it under a salt stress condition. Consistently, there was a drastic but transient decrease in the intracellular amount of RsgA after salt shock. Salt shock would make the pathway of maturation of the ribosome small subunit RsgA independent.
RsgA是一种独特的GTP水解蛋白，其GTP酶活性被小核糖体亚基显著增强。RsgA的缺失导致细胞生长缓慢以及核糖体亚基组装和16S rRNA加工缺陷，表明它参与小亚基的成熟。在本研究中，我们发现去除RsgA或使其核糖体小亚基依赖性GTP酶活性失活可使大肠杆菌细胞对高盐胁迫产生抗性。盐胁迫抑制了RsgA缺失细胞中核糖体亚基组装、16S rRNA加工以及16S rRNA 3'端截短的缺陷。相反，盐胁迫短暂损害了野生型细胞中核糖体亚基组装和16S rRNA加工，并诱导了16S rRNA的3'端截短。这些结果表明，RsgA通常促进小亚基成熟的对核糖体的作用在盐胁迫条件下会受到干扰。一致地，盐休克后细胞内RsgA的量急剧但短暂地减少。盐休克会使核糖体小亚基的成熟途径独立于RsgA。
