van Alphen W, Lugtenberg B, Berendsen W
Mol Gen Genet. 1976 Sep 23;147(3):263-9. doi: 10.1007/BF00582877.
Mutants of Escherichia coli K12, deficient in up to three major outer membrane proteins b, c and d have been constructed. Mutants that lack the lipopolysaccharide sugar heptose are deficient in protein b. All heptose-deficient strains are supersensitive to lysozyme, various antibiotics and detergents. They excrete the periplasmic enzyme ribonuclease I. Mutants deficient in proteins c and/or d have the same sensitivity towards these compounds as the parent strain. Cells of single, double and triple mutants are all rod-shaped. Electrophoretic analysis of cell envelope proteins indicates that in some mutants the protein deficiency is partially compensated for by increased amounts of one or two of the other major outer membrane proteins. Heptose-deficient strains have an increased amount of 2-keto-3-deoxyoctonate.
已构建出大肠杆菌K12的突变体,这些突变体缺失多达三种主要外膜蛋白b、c和d。缺乏脂多糖庚糖的突变体缺乏蛋白b。所有庚糖缺陷型菌株对溶菌酶、各种抗生素和去污剂超敏感。它们会分泌周质酶核糖核酸酶I。缺乏蛋白c和/或d的突变体对这些化合物的敏感性与亲本菌株相同。单突变体、双突变体和三突变体的细胞均为杆状。对细胞包膜蛋白的电泳分析表明,在一些突变体中,一种或两种其他主要外膜蛋白数量的增加可部分弥补蛋白质缺陷。庚糖缺陷型菌株的2-酮-3-脱氧辛酸含量增加。