Kusser W, Ishiguro E E
J Bacteriol. 1987 Sep;169(9):4396-8. doi: 10.1128/jb.169.9.4396-4398.1987.
Mutations in Escherichia coli previously reported (R. E. Harkness and E. E. Ishiguro, J. Bacteriol. 155:15-21, 1983; L. C. Shimmin, D. Vanderwel, R. E. Harkness, B. R. Currie, A. Galloway, and E. E. Ishiguro, J. Gen. Microbiol. 130:1315-1323, 1984) as conferring a temperature-dependent tolerance to lysis induced by inhibitors of peptidoglycan synthesis were suppressed by treatment with inhibitors of the stringent response or by introduction of a relA mutation. The relA+ derivatives of the mutants exhibited a stringent response at the nonpermissive temperature. The consequent inhibition of the autolytic enzyme system (W. Kusser and E. E. Ishiguro, J. Bacteriol. 164:861-865, 1985) was apparently responsible for the lysis-tolerant phenotypes of these mutants.
先前报道的大肠杆菌中的突变（R. E. 哈克尼斯和E. E. 石黑，《细菌学杂志》155:15 - 21，1983年；L. C. 希明、D. 范德韦尔、R. E. 哈克尼斯、B. R. 柯里、A. 加洛韦和E. E. 石黑，《普通微生物学杂志》130:1315 - 1323，1984年）赋予了对肽聚糖合成抑制剂诱导的裂解的温度依赖性耐受性，用严紧反应抑制剂处理或引入relA突变可抑制这种耐受性。突变体的relA +衍生物在非允许温度下表现出严紧反应。由此对自溶酶系统的抑制（W. 库瑟和E. E. 石黑，《细菌学杂志》164:861 - 865，1985年）显然是这些突变体的裂解耐受表型的原因。
