Eidels L, Osborn M J
Proc Natl Acad Sci U S A. 1971 Aug;68(8):1673-7. doi: 10.1073/pnas.68.8.1673.
Genetic and biochemical evidence that sedoheptulose-7-phosphate is an obligatory precursor of the L-glycero-D-mannoheptose residues of the lipopolysaccharide of Salmonella was obtained by isolation and characterization of transketolase-negative mutants of Salmonella typhimurium. These mutants, which are defective in synthesis of sedoheptulose-7-phosphate, were found to produce an incomplete heptose-deficient lipopolysaccharide, and were also sensitive to bile salts, a characteristic property of heptose-deficient mutants. Phenotypic repair of the defect in lipopolysaccharide synthesis was obtained by addition of exogenous sedoheptulose-7-phosphate to growing cultures of the mutant strains. Characterization of revertants isolated either as transketolase-positive or heptose-positive provided further evidence that the heptose deficiency resulted from mutation at the transketolase locus. On the basis of these findings a possible pathway for conversion of sedoheptulose-7-phosphate to L-glycero-D-mannoheptose is proposed.
通过对鼠伤寒沙门氏菌转酮醇酶阴性突变体的分离和鉴定,获得了遗传和生化证据,证明景天庚酮糖-7-磷酸是沙门氏菌脂多糖中L-甘油-D-甘露庚糖残基的必需前体。这些在景天庚酮糖-7-磷酸合成方面存在缺陷的突变体,被发现产生不完全的庚糖缺陷型脂多糖,并且对胆盐敏感,这是庚糖缺陷型突变体的一个特征性特性。通过向突变菌株的生长培养物中添加外源性景天庚酮糖-7-磷酸,获得了脂多糖合成缺陷的表型修复。对分离得到的转酮醇酶阳性或庚糖阳性回复突变体的鉴定提供了进一步的证据,表明庚糖缺陷是由转酮醇酶基因座的突变引起的。基于这些发现,提出了一条将景天庚酮糖-7-磷酸转化为L-甘油-D-甘露庚糖的可能途径。