Mäkelä P H
J Bacteriol. 1973 Nov;116(2):847-56. doi: 10.1128/jb.116.2.847-856.1973.
In salmonella O group B, the O antigen factor 12(2) is created by glucosylation at C4 of the galactose units of the O side chains; phage-determined glucosylation at C6 of these galactose units yields factor 1. 12(2)-negative mutants were isolated from 12(2) (+) (stable) parents (genetically oafR(+st)). All 20 mutants studied were stable in respect of their 12(2) character. In eight of them, lysogenization by phage P22 resulted in the appearance of the 12(2) factor-these were interpreted to be defective in the enzyme(s) needed to synthesize the glucose-lipid intermediate that participates in both 12(2)- and 1-specific glucosylation; the corresponding cistron was termed oafE. This "complementation" assay also demonstrated that the P22 genome can determine the synthesis of this glucose-lipid intermediate. The 12(2) character in the oafE(-) mutants became variable after P22 lysogenization, corresponding to factor 1 variation normally determined by this phage. In the remaining 12 mutants, P22 caused the appearance of a variable factor 1, but not of 12(2). The lesion in all the 12(2) mutants was mapped close to the gene purE at min 19 of the Salmonella map. This is the same area where the locus oafR that controls the variation (stable or variable, + or -) of 12(2) had been previously mapped. The results suggest the presence of a 12(2) glucosylation operon in this region.
在沙门氏菌O群B中,O抗原因子12(2)是由O侧链半乳糖单元C4位的糖基化作用产生的;这些半乳糖单元C6位由噬菌体决定的糖基化作用产生因子1。从12(2)(稳定型)亲本(基因型为oafR(+st))中分离出12(2)阴性突变体。所研究的20个突变体在其12(2)特性方面都是稳定的。其中8个突变体经噬菌体P22溶原化后出现了12(2)因子——这些突变体被认为在合成参与12(2)和1特异性糖基化的葡萄糖-脂质中间体所需的酶方面存在缺陷;相应的顺反子被称为oafE。这种“互补”试验还表明,P22基因组可以决定这种葡萄糖-脂质中间体的合成。oafE(-)突变体中的12(2)特性在P22溶原化后变得可变,这与该噬菌体通常决定的因子1变异相对应。在其余12个突变体中,P22导致出现可变的因子1,但没有出现12(2)因子。所有12(2)突变体中的损伤都定位在沙门氏菌染色体图谱第19分钟处靠近purE基因的位置。这与之前定位的控制12(2)变异(稳定或可变,+或-)的oafR基因座在同一区域。结果表明该区域存在一个12(2)糖基化操纵子。