Whitfield C, Schoenhals G, Graham L
Department of Microbiology, College of Biological Sciences, University of Guelph, Ontario, Canada.
J Gen Microbiol. 1989 Oct;135(10):2589-99. doi: 10.1099/00221287-135-10-2589.
Escherichia coli K30 produces a thermostable group I capsular polysaccharide. Two classes of mutants were isolated with defects in the synthesis or expression of capsule. The most common mutant phenotype was acapsular (K-), with no K-antigen synthesized. A second class of mutants, termed Ki or intermediate forms, produced colonies which were indistinguishable from those of acapsular forms yet K-antigenicity was expressed. Previous studies had demonstrated that E. coli strains that produce K30 antigen synthesize a lipopolysaccharide (LPS) fraction that is recognised by monoclonal antibodies against the K30 antigen. Synthesis of this LPS fraction was not affected in Ki forms. The results of morphological examination, LPS analysis and phage sensitivity studies are consistent with the interpretation that the defect in Ki strains results from an inability to polymerize the K30 antigen. Using plasmid pULB113 (RP4::mini-Mu), mutations resulting in both K- and Ki phenotypes were localized near the his region of the chromosome.
大肠杆菌K30产生一种热稳定的I类荚膜多糖。分离出了两类在荚膜合成或表达方面存在缺陷的突变体。最常见的突变体表型是无荚膜(K-),不合成K抗原。第二类突变体,称为Ki或中间型,产生的菌落与无荚膜型的菌落无法区分,但表达K抗原性。先前的研究表明,产生K30抗原的大肠杆菌菌株合成一种脂多糖(LPS)组分,该组分可被抗K30抗原的单克隆抗体识别。这种LPS组分的合成在Ki型中不受影响。形态学检查、LPS分析和噬菌体敏感性研究的结果与以下解释一致,即Ki菌株的缺陷是由于无法聚合K30抗原所致。利用质粒pULB113(RP4::mini-Mu),导致K-和Ki表型的突变定位在染色体的his区域附近。