Zimmermann R A, Ikeya Y, Sparling P F
Proc Natl Acad Sci U S A. 1973 Jan;70(1):71-5. doi: 10.1073/pnas.70.1.71.
An alteration in the chromatographic mobility of 30S ribosomal protein S4 from two kasugamycin-resistant (ksgA) strains of E. coli was observed. The locus determining this alteration frequently cotransduced with ksgA but could be separated from it by transduction and conjugation. Since the structural gene for protein S4 is thought to lie some 30 min from ksgA on the E. coli chromosome, the product of the newly-identified gene may modify protein S4. We propose to designate this gene ramB.Reconstitution of 30S subunits from RNA and protein components of ksgA ramB and ksgA(+)ramB(+) strains demonstrated that ribosomal resistance to kasugamycin was due to altered 16S RNA and not to altered protein S4. The altered 16S RNA was undermethylated, and a methylating enzyme that acts on 16S RNA from ksgA strains was present in ksgA(+) but not in ksgA strains.
观察到来自两株抗春日霉素(ksgA)的大肠杆菌菌株的30S核糖体蛋白S4的色谱迁移率发生了改变。决定这种改变的基因座经常与ksgA共转导,但可以通过转导和接合将其与ksgA分离。由于蛋白S4的结构基因被认为位于大肠杆菌染色体上距离ksgA约30分钟处,新鉴定基因的产物可能会修饰蛋白S4。我们提议将该基因命名为ramB。从ksgA ramB和ksgA(+)ramB(+)菌株的RNA和蛋白质组分重建30S亚基表明,核糖体对春日霉素的抗性是由于16S RNA改变而非蛋白S4改变所致。改变的16S RNA甲基化不足,并且一种作用于ksgA菌株16S RNA的甲基化酶存在于ksgA(+)菌株中而不存在于ksgA菌株中。