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青霉素酶合成的调控:金黄色葡萄球菌中一个与青霉素酶质粒不连锁的突变降低了青霉素酶的诱导性。

Regulation of penicillinase synthesis: a mutation in Staphylococcus aureus unlinked to the penicillinase plasmid that reduced penicillinase inducibility.

作者信息

Zyskind J W, Imsande J

出版信息

J Bacteriol. 1972 Jan;109(1):116-21. doi: 10.1128/jb.109.1.116-121.1972.

Abstract

A mutant of Staphylococcus aureus strain 655 was isolated that is restricted in penicillinase induction. Wild-type plasmids that bear penicillinase determinants could not be fully induced in this mutant, 655par-1; hence, the responsible mutation is not located on the plasmid. Mutant plasmid PI(258)penI443, which produces penicillinase constitutively in wild-type cells, was fully constitutive for penicillinase production when it was harbored by mutant 655par-1. Therefore, the bacterial mutation does not interfere directly with the transcription of the penZ gene or translation of the penicillinase messenger ribonucleic acid. Mutant plasmid PII(147)penI220 was fully inducible in the mutant bacterium, even though the wild-type plasmid PII(147) was only partially inducible in the par-1 mutant. Thus, in the presence of inducer, complementation appears to occur between the product of the par-1 gene and the product of the penI220 gene. These results suggest that the par-1 gene codes for a penicillinase antire-pressor.

摘要

分离出一株金黄色葡萄球菌655的突变体,其青霉素酶诱导受到限制。携带青霉素酶决定簇的野生型质粒在该突变体655par - 1中不能被完全诱导;因此,相关突变不在质粒上。突变体质粒PI(258)penI443在野生型细胞中组成性产生青霉素酶,当它被突变体655par - 1携带时,青霉素酶产生完全呈组成型。所以,细菌突变并不直接干扰penZ基因的转录或青霉素酶信使核糖核酸的翻译。突变体质粒PII(147)penI220在突变细菌中是完全可诱导的,尽管野生型质粒PII(147)在par - 1突变体中只是部分可诱导。因此,在诱导剂存在的情况下,par - 1基因的产物与penI220基因的产物之间似乎发生了互补作用。这些结果表明par - 1基因编码一种青霉素酶抗阻遏物。

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Regulation of staphylococcal penicillinase synthesis.葡萄球菌青霉素酶合成的调控
J Bacteriol. 1972 Jan;109(1):122-33. doi: 10.1128/jb.109.1.122-133.1972.

引用本文的文献

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Regulation of staphylococcal penicillinase synthesis.葡萄球菌青霉素酶合成的调控
J Bacteriol. 1972 Jan;109(1):122-33. doi: 10.1128/jb.109.1.122-133.1972.

本文引用的文献

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Iodometric assay of penicillinase.青霉素酶的碘量法测定
Nature. 1954 Nov 27;174(4439):1012-3. doi: 10.1038/1741012a0.

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