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肺炎球菌中四环素耐药性的分子机制。

The molecular mechanisms of tetracycline resistance in the pneumococcus.

作者信息

Widdowson C A, Klugman K P

机构信息

South African Institute for Medical Research and the University of Witwatersrand, Department of Clinical Microbiology and Infectious Diseases, Johannesburg.

出版信息

Microb Drug Resist. 1998 Spring;4(1):79-84. doi: 10.1089/mdr.1998.4.79.

DOI:10.1089/mdr.1998.4.79
PMID:9533730
Abstract

Tetracycline resistance in the pneumococcus is a result of the acquisition of one of two resistance determinants, tet(M) or tet(O). These genes encode ribosomal protection proteins that have homology to the elongation factors G and Tu. Tet(M) and Tet(O) both have GTPase activity that appears to be important in the displacement of tetracycline from the ribosome. Modification of tRNA may also be important for tetracycline resistance. Transcription of tet(M) is thought to be regulated by transcriptional attenuation. Transcription of tet(O) is constitutive, however, upstream of the gene are sequences that also appear to be involved in transcriptional attenuation. tet(M) is transferred on the conjugative transposons, Tn1545 and Tn5151. It is not yet known whether tet(O) is transported on transposons or plasmids, or whether it is chromosomally integrated, in pneumococci.

摘要

肺炎球菌对四环素的耐药性是获得两种耐药决定因素tet(M)或tet(O)之一的结果。这些基因编码与延伸因子G和Tu具有同源性的核糖体保护蛋白。Tet(M)和Tet(O)都具有GTPase活性,这似乎在四环素从核糖体上的置换中起重要作用。tRNA的修饰对于四环素耐药性可能也很重要。tet(M)的转录被认为受转录衰减调控。然而,tet(O)的转录是组成型的,不过在该基因上游存在似乎也参与转录衰减的序列。tet(M)通过接合转座子Tn1545和Tn5151进行转移。目前尚不清楚tet(O)在肺炎球菌中是通过转座子还是质粒进行转运,或者它是否整合到染色体上。

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