Kuhn M, Goebel W
Institut für Genetik und Mikrobiologie, Universität Würzburg, Federal Republic of Germany.
Infect Immun. 1989 Jan;57(1):55-61. doi: 10.1128/iai.57.1.55-61.1989.
Mutants of Listeria monocytogenes were recently isolated which are impaired in the synthesis of a major extracellular protein (p60). As shown in this investigation, the p60 mutants have lost the capability of invading nonprofessional phagocytic 3T6 mouse fibroblast cells. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of supernatant proteins of these mutants indicated that no other extracellular protein was altered in these mutants. The p60 mutants formed long cell chains which disaggregated to normal-sized single bacteria upon treatment with partially purified p60. These disaggregated bacterial cells were able to invade 3T6 cells. Physical disruption of the cell chains by ultrasonication produced similar single cells which were, however, noninvasive. Treatment of these ultrasonicated mutant cells with wild-type p60 restored their ability to invade 3T6 cells.
最近分离出了单核细胞增生李斯特菌的突变体,这些突变体在一种主要细胞外蛋白(p60)的合成上存在缺陷。如本研究所示,p60突变体失去了侵入非专职吞噬性3T6小鼠成纤维细胞的能力。对这些突变体的上清液蛋白进行十二烷基硫酸钠-聚丙烯酰胺凝胶电泳表明,这些突变体中没有其他细胞外蛋白发生改变。p60突变体形成长细胞链,在用部分纯化的p60处理后,这些细胞链会解聚为正常大小的单个细菌。这些解聚的细菌细胞能够侵入3T6细胞。通过超声处理对细胞链进行物理破坏会产生类似的单个细胞,然而这些细胞没有侵袭能力。用野生型p60处理这些经超声处理的突变体细胞可恢复它们侵入3T6细胞的能力。