Aseev Leonid V, Levandovskaya Alexandrina A, Tchufistova Ludmila S, Scaptsova Nadezda V, Boni Irina V
Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997, Moscow, Russia.
RNA. 2008 Sep;14(9):1882-94. doi: 10.1261/rna.1099108. Epub 2008 Jul 22.
Autogenous regulation is a general strategy of balancing ribosomal protein synthesis in bacteria. Control mechanisms have been studied in detail for most of ribosomal protein operons, except for rpsB-tsf encoding essential r-protein S2 and elongation factor Ts, where even the promoter has remained unknown. By using single-copy translational fusions with the chromosomal lacZ gene and Western-blot analysis, we demonstrate here that S2 serves as a negative regulator of both rpsB and tsf expression in vivo, acting at a single target within the rpsB 5'-untranslated region (5'-UTR). As determined by primer extension, transcription of the Escherichia coli rpsB-tsf operon starts 162 nucleotides upstream of the rpsB initiation codon at a single promoter TGTGGTATAAA belonging to the extended -10 promoter class. Both the promoter signature and the 5'-UTR structure of the rpsB gene appear to be highly conserved in gamma-proteobacteria. Deletion analysis of the rpsB 5'-UTR within rpsB'-'lacZ fusions has revealed that an operator region involved in the S2 autoregulation comprises conserved structural elements located upstream of the rpsB ribosome binding site. The S2-mediated autogenous control is impaired in rpsB mutants and, more surprisingly, in the rpsA mutant producing decreased amounts of truncated r-protein S1 (rpsAIS10), indicating that S2 might act as a repressor in cooperation with S1.
自体调控是细菌中平衡核糖体蛋白合成的一种普遍策略。除了编码必需核糖体蛋白S2和延伸因子Ts的rpsB - tsf外,大多数核糖体蛋白操纵子的控制机制已得到详细研究,而rpsB - tsf的启动子甚至仍不为人知。通过使用与染色体lacZ基因的单拷贝翻译融合和蛋白质免疫印迹分析,我们在此证明S2在体内作为rpsB和tsf表达的负调控因子,作用于rpsB 5' - 非翻译区(5' - UTR)内的单一靶点。通过引物延伸确定,大肠杆菌rpsB - tsf操纵子的转录在rpsB起始密码子上游162个核苷酸处开始,起始于一个属于扩展 -10启动子类别的单一启动子TGTGGTATAAA。rpsB基因的启动子特征和5' - UTR结构在γ - 变形菌中似乎高度保守。对rpsB' - 'lacZ融合体中rpsB 5' - UTR的缺失分析表明,参与S2自体调控的一个操纵子区域包含位于rpsB核糖体结合位点上游的保守结构元件。S2介导的自体调控在rpsB突变体中受损,更令人惊讶的是,在产生截短核糖体蛋白S1(rpsAIS10)量减少的rpsA突变体中也受损,这表明S2可能与S1协同作为阻遏物发挥作用。