Mäkelä P H, Mayer H, Whang H Y, Neter E
J Bacteriol. 1974 Sep;119(3):760-4. doi: 10.1128/jb.119.3.760-764.1974.
A series of R (rough) Salmonella minnesota mutants with rfb, rfe, and rfa mutations leading to various defects in the biosynthesis of cell wall lipopolysaccharide was analyzed as to their enterobacterial common antigen (CA) content. All mutants that had functional rfe genes were CA(+) as is the wild-type parent. This includes mutants with the most defective lipopolysaccharide core types, demonstrating that core structures are not a necessary part of CA. All rfe(-) mutants (complete lipopolysaccharide core, defective synthesis of O side chains) were defective in the synthesis of CA. A smooth strain was accidentally found to be CA(-); the mutation responsible for this defect was also located, like rfe, very close to ilv.
分析了一系列具有rfb、rfe和rfa突变的粗糙型明尼苏达沙门氏菌突变体，这些突变导致细胞壁脂多糖生物合成出现各种缺陷，并检测了它们的肠道细菌共同抗原（CA）含量。所有具有功能性rfe基因的突变体，如同野生型亲本一样，都是CA(+)。这包括脂多糖核心类型缺陷最严重的突变体，表明核心结构不是CA的必要组成部分。所有rfe(-)突变体（完整的脂多糖核心，O侧链合成缺陷）在CA合成方面存在缺陷。偶然发现一株光滑型菌株是CA(-)；导致这种缺陷的突变，如同rfe一样，也定位在非常靠近ilv的位置。
