Hurst A, Hughes A
Can J Microbiol. 1981 Jun;27(6):627-32. doi: 10.1139/m81-095.
Sublethal heating of Staphylococcus aureus S6 in potassium phosphate buffer caused loss of salt tolerance, D-alanine, and magnesium. During incubation in rich complex media all three of the damaged sites were repaired. Repair occurred more slowly but went to completion in a dilute synthetic medium (DSM), free of D-ala. DSM plus penicillin or D-cycloserine allowed repair of salt tolerance but recovery of normal levels of D-ala or Mg was prevented. When DSM-repaired cells were cultured into fresh rich medium they grew rapidly after a short lag. Cells which had acquired their salt tolerance in DSM plus cycloserine and were D-ala and Mg deficient grew slowly and had a lag of 3 h. We suggest that heat damage has two separate primary targets in S. aureus cells: the membrane, which is manifested by loss of salt tolerance, and a second site, possibly teichoic acids, manifested by loss of D-ala and Mg.
在磷酸钾缓冲液中对金黄色葡萄球菌S6进行亚致死加热会导致其耐盐性、D - 丙氨酸和镁的丧失。在丰富的复合培养基中培养期间,所有这三个受损部位都得到了修复。在不含D - 丙氨酸的稀释合成培养基(DSM)中修复发生得更慢,但最终完成。DSM加上青霉素或D - 环丝氨酸可使耐盐性得到修复,但阻止了D - 丙氨酸或镁恢复到正常水平。当将DSM修复的细胞接种到新鲜的丰富培养基中时,它们在短暂的延迟后迅速生长。在DSM加环丝氨酸中获得耐盐性且缺乏D - 丙氨酸和镁的细胞生长缓慢,并有3小时的延迟期。我们认为热损伤在金黄色葡萄球菌细胞中有两个独立的主要靶点:膜,表现为耐盐性丧失;另一个位点,可能是磷壁酸,表现为D - 丙氨酸和镁的丧失。