Lithgow James K, Ingham Eileen, Foster Simon J
Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield S10 2TN, UK.
Department of Microbiology, University of Leeds, Leeds LS2 9JT, UK.
Microbiology (Reading). 2004 Feb;150(Pt 2):373-381. doi: 10.1099/mic.0.26674-0.
The roles of two adjacent genes in the Staphylococcus aureus chromosome with functions in starvation survival and the response to stressful conditions have been characterized. One of these, hprT, encoding a hypoxanthine-guanine phosphoribosyltransferase homologue, was initially identified in a transposon mutagenesis screen. Mutation of hprT affects starvation survival in amino-acid-limiting conditions and the ability of S. aureus to grow in high-salt concentrations. Downstream of hprT is ftsH, which encodes a membrane-bound, ATP- and Zn(2+)-dependent 'AAA'-type protease. Mutation of ftsH in S. aureus leads to pleiotropic defects including slower growth, sensitivity to salt, acid, methyl viologen and potassium tellurite stresses, and reduced survival in amino-acid- or phosphate-limiting conditions. Both hprT-lacZ and ftsH-lacZ gene fusions are expressed maximally in the post-exponential phase of growth. Although secretion of exoproteins is not affected, an ftsH mutant is attenuated in a murine skin lesion model of pathogenicity.
已对金黄色葡萄球菌染色体上两个相邻基因的作用进行了表征,这两个基因在饥饿存活及应激条件反应中发挥作用。其中一个基因hprT编码次黄嘌呤 - 鸟嘌呤磷酸核糖基转移酶同源物,最初是在转座子诱变筛选中被鉴定出来的。hprT突变会影响在氨基酸限制条件下的饥饿存活以及金黄色葡萄球菌在高盐浓度下生长的能力。hprT的下游是ftsH,它编码一种膜结合的、依赖ATP和Zn(2+)的“AAA”型蛋白酶。金黄色葡萄球菌中ftsH的突变会导致多效性缺陷,包括生长缓慢、对盐、酸、甲基紫精和亚碲酸钾应激敏感,以及在氨基酸或磷酸盐限制条件下存活率降低。hprT - lacZ和ftsH - lacZ基因融合体在生长的指数后期阶段表达量最高。虽然外蛋白的分泌不受影响,但ftsH突变体在致病性小鼠皮肤损伤模型中毒力减弱。