Lew H C, Nikaido H, Mäkelä P H
J Bacteriol. 1978 Oct;136(1):227-33. doi: 10.1128/jb.136.1.227-233.1978.
In Salmonella typhimurium, three groups of genes located in rfb, rfe, and rff clusters are known to be involved in the biosynthesis of the enterobacterial common antigen. We found that enzymatic synthesis of uridine diphosphate N-acetylmannosaminouric acid, the activated form of a constituent sugar of the common antigen, followed the pathway previously described in Escherichia coli (N. Ichihara, N. Ishimoto, and E. Ito, FEBS Lett. 39:46--48, 1974). All of the six rff mutants tested, which fail to synthesize the common antigen, were deficient in one or both of the two enzymes needed for the synthesis of this sugar nucleotide from uridine diphosphate N-acetylglucosamine; these results established the physiological role of the pathway studied for the biosynthesis of N-acetylmannosaminuronic acid residues. The levels of these enzymes were not reduced in rfe mutants or rfb deletion mutants, although they produced no or only traces of the common antigen.
在鼠伤寒沙门氏菌中，已知位于rfb、rfe和rff簇中的三组基因参与肠道细菌共同抗原的生物合成。我们发现，尿苷二磷酸N-乙酰甘露糖胺糖醛酸（共同抗原的一种组成糖的活化形式）的酶促合成遵循先前在大肠杆菌中描述的途径（N. 市原、N. 石本和E. 伊藤，《欧洲生物化学学会联合会快报》39:46 - 48，1974年）。所测试的六个rff突变体均不能合成共同抗原，它们在从尿苷二磷酸N-乙酰葡糖胺合成这种糖核苷酸所需的两种酶中的一种或两种上存在缺陷；这些结果确定了所研究的途径在N-乙酰甘露糖胺糖醛酸残基生物合成中的生理作用。尽管rfe突变体或rfb缺失突变体不产生或仅产生微量的共同抗原，但这些酶的水平并未降低。
