Sato S, Ishikawa H
Department of Biological Sciences, Graduate School of Science, University of Tokyo, Japan.
J Bacteriol. 1997 Apr;179(7):2300-4. doi: 10.1128/jb.179.7.2300-2304.1997.
Members of the genus Buchnera are intracellular symbionts harbored by the aphid bacteriocyte which selectively synthesize symbionin, a homolog of the Escherichia coli GroEL protein, in vivo. Symbionin and SymS, a GroES homolog, are encoded in the symSL operon. Northern blotting and primer extension analyses revealed that the symSL operon invariably gives rise to a bicistronic mRNA under the control of a heat shock promoter, though the amount of the symSL mRNA in the isolated symbiont did not increase in response to heat shock. The sigma32 protein that recognizes the heat shock promoter in E. coli was scarcely detected in Buchnera cells even after heat shock. Although the functionally essential regions of the Buchnera sigma32 protein were well conserved, the Buchnera rpoH gene did not complement an E. coli delta rpoH mutant. On the one hand, the A-T evolutionary pressure imposed on the Buchnera genome may have not only decreased the activity of its sigma32 but also ruined the nucleotide sequences necessary for the expression of rpoH; on the other hand, it may have facilitated expression of the symSL operon without activation by sigma32.
布赫纳氏菌属的成员是蚜虫菌细胞内寄生的共生体,它们在体内选择性地合成共生蛋白,这是一种大肠杆菌GroEL蛋白的同源物。共生蛋白和GroES同源物SymS由symSL操纵子编码。Northern印迹和引物延伸分析表明,symSL操纵子在热休克启动子的控制下总是产生双顺反子mRNA,尽管分离出的共生体中symSL mRNA的量在热休克后并没有增加。即使在热休克后,在布赫纳氏菌细胞中也几乎检测不到识别大肠杆菌热休克启动子的sigma32蛋白。虽然布赫纳氏菌sigma32蛋白的功能必需区域高度保守,但布赫纳氏菌rpoH基因不能互补大肠杆菌的delta rpoH突变体。一方面,施加在布赫纳氏菌基因组上的A-T进化压力可能不仅降低了其sigma32的活性,还破坏了rpoH表达所需的核苷酸序列;另一方面,它可能促进了symSL操纵子在没有sigma32激活的情况下的表达。