Wollin R, Creeger E S, Rothfield L I, Stocker B A, Lindberg A A
J Biol Chem. 1983 Mar 25;258(6):3769-74.
The biochemical defect in a class of Salmonella typhimurium mutants (rfaB) defective in biosynthesis of the lipopolysaccharide core is described. Structural, immunochemical and enzymologic studies showed that: (i) the core polysaccharide completely lacked the branch alpha 1,6-D-galactosyl residue of the normal lipopolysaccharide as shown by methylation analysis and 1H nmr spectroscopy; (ii) the mutant lipopolysaccharides acted as acceptors for transfer of D-galactose from UDP-D-galactose into alpha 1,6 linkage to the proximal D-glucosyl residue of the core in a reaction catalyzed by an enzyme activity present in extracts from rfaB+ cells; (iii) the UDP-D-galactose:(glucosyl)lipopolysaccharide alpha 1,6-D-galactosyltransferase activity was absent from extracts of rfaB cells.
描述了一类鼠伤寒沙门氏菌突变体(rfaB)在脂多糖核心生物合成方面存在缺陷的生化缺陷。结构、免疫化学和酶学研究表明:(i)通过甲基化分析和1H核磁共振光谱显示,核心多糖完全缺乏正常脂多糖的分支α1,6-D-半乳糖基残基;(ii)在由rfaB+细胞提取物中存在的酶活性催化的反应中,突变体脂多糖作为受体,用于将UDP-D-半乳糖中的D-半乳糖转移至核心近端D-葡萄糖基残基上形成α1,6连接;(iii)rfaB细胞提取物中不存在UDP-D-半乳糖:(葡萄糖基)脂多糖α1,6-D-半乳糖基转移酶活性。