Lipsett M N
J Bacteriol. 1978 Sep;135(3):993-7. doi: 10.1128/jb.135.3.993-997.1978.
A previously described mutant of Escherichia coli which lacks 4-thiouridine in its tRNA was here shown to be deficient in factor A, one of the two proteins responsible for this thiolation of uridine. Addition of exogenous factor A restored the thiolating ability of extracts prepared from the mutant. The activities of the two thiolation proteins were governed by genes at two widely separated positions on the chromosome, as determined with F-prime merodiploids. The site governing factor A activity lay roughly in the region of the recently reported position of nuv, a gene controlling the production of 4-thiouridine in tRNA.
先前描述的一种大肠杆菌突变体,其转运核糖核酸(tRNA)中缺乏4-硫尿苷,在本文中显示它缺乏因子A,因子A是负责尿苷这种硫醇化修饰的两种蛋白质之一。添加外源因子A可恢复从该突变体制备的提取物的硫醇化能力。如用F-prime部分二倍体所测定,这两种硫醇化蛋白质的活性受位于染色体上两个相距很远位置的基因控制。控制因子A活性的位点大致位于最近报道的nuv基因位置区域,nuv基因控制tRNA中4-硫尿苷的产生。