de Jonge B L, de Lencastre H, Tomasz A
Rockefeller University, New York, New York 10021.
J Bacteriol. 1991 Feb;173(3):1105-10. doi: 10.1128/jb.173.3.1105-1110.1991.
Isogenic Tn551 mutants of a highly and uniformly methicillin-resistant strain of Staphylococcus aureus were tested for their rates of autolysis and cell wall degradation in buffer and for cell wall turnover during growth. The normal (relatively fast) autolysis and turnover rates of the parent strain were retained in a Tn551 mutant in which the insert was located within the mec gene and which produced undetectable levels of penicillin-binding protein 2A. On the other hand, autolysis and cell wall turnover rates were greatly reduced in auxiliary mutants, i.e., mutants in which the transposon caused conversion of the high-level and uniform resistance of the parent strain to a variety of distinct heterogeneous expression types and greatly decreased resistance levels. All of these mutants contained an intact mec gene and produced normal amounts of penicillin-binding protein 2A, and one of the mutations was located in the femA region of the staphylococcal chromosome (B. Berger-Bachi, L. Barberis-Maino, A. Strassle, and F. H. Kayser, Mol. Gen. Genet. 219:263-269, 1989). Autolysis rates were related to the degree of residual methicillin resistance and to the sites of Tn551 insertion. Fast cell wall turnover may help expression of high-level methicillin resistance by providing a mechanism for the excision of abnormal (and potentially lethal) structural elements of the cell wall synthesized by the bacteria in the presence of methicillin.
对一株高度且均匀耐甲氧西林的金黄色葡萄球菌的同基因Tn551突变体进行了测试,检测它们在缓冲液中的自溶速率和细胞壁降解情况,以及生长过程中的细胞壁周转情况。亲本菌株正常(相对较快)的自溶和周转速率在一个Tn551突变体中得以保留,该突变体中插入片段位于mec基因内,且产生的青霉素结合蛋白2A水平无法检测到。另一方面,在辅助突变体中,自溶和细胞壁周转速率大大降低,即这些突变体中,转座子导致亲本菌株的高水平和均匀抗性转变为多种不同的异质表达类型,且抗性水平大幅下降。所有这些突变体都含有完整的mec基因,产生正常量的青霉素结合蛋白2A,其中一个突变位于葡萄球菌染色体的femA区域(B. Berger-Bachi、L. Barberis-Maino、A. Strassle和F. H. Kayser,《分子与普通遗传学》219:263 - 269,1989)。自溶速率与残余甲氧西林抗性程度以及Tn551插入位点有关。快速的细胞壁周转可能通过提供一种机制来切除细菌在甲氧西林存在下合成的细胞壁异常(且可能致命)结构元件,从而有助于高水平甲氧西林抗性的表达。