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一个编码组成型大环内酯-林可酰胺-链阳菌素B耐药性的金黄色葡萄球菌质粒在ermC弱化子中存在一个新的缺失。

A Staphylococcus aureus plasmid that specifies constitutive macrolide-lincosamide-streptogramin B resistance contains a novel deletion in the ermC attenuator.

作者信息

Catchpole I, Dyke K G

机构信息

Department of Biochemistry, University of Oxford, U.K.

出版信息

FEMS Microbiol Lett. 1990 May;57(1-2):43-7. doi: 10.1016/0378-1097(90)90410-r.

Abstract

A 2.5 kb plasmid, pA22, isolated from a naturally occurring S. aureus strain confers constitutive MLS-resistance. By restriction enzyme analysis, pA22 is indistinguishable from the S. aureus inducible MLS-resistance conferring plasmid, pT48, apart froma small deletion. DNA sequencing showed that the deletion, is in the leader/attenuator region of the ermC (MLS-resistance) gene and removes some of the complementary repeat regions required by the translational attenuation model in pT48 for inducible ermC expression. The deletion in plasmid pA22 is different from that found in similar 2.5kb constitutive MLS-resistance plasmids in other Gram-positive bacteria. It is suggested that plasmids conferring the constitutive phenotype have evolved from an inducible ancestor on several independent occasions.

摘要

从一株天然存在的金黄色葡萄球菌中分离出的2.5 kb质粒pA22可赋予组成型大环内酯-林可酰胺-链阳霉素B(MLS)抗性。通过限制性内切酶分析,除了一个小的缺失外,pA22与赋予金黄色葡萄球菌诱导型MLS抗性的质粒pT48无法区分。DNA测序表明,该缺失位于ermC(MLS抗性)基因的前导/弱化子区域,并去除了pT48中翻译衰减模型诱导ermC表达所需的一些互补重复区域。质粒pA22中的缺失与其他革兰氏阳性细菌中类似的2.5 kb组成型MLS抗性质粒中的缺失不同。有人提出,赋予组成型表型的质粒是在几个独立的情况下从可诱导的祖先进化而来的。

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