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肺炎链球菌转座子 Tn1545/Tn6003 通过 erm(B)-和 aphA3 编码的大环内酯-氨基糖苷-链霉菌(MAS)元件的圆形自发缺失,转变为 Tn6002。

Streptococcus pneumoniae transposon Tn1545/Tn6003 changes to Tn6002 due to spontaneous excision in circular form of the erm(B)- and aphA3-containing macrolide-aminoglycoside-streptothricin (MAS) element.

机构信息

Unit of Microbiology, Department of Biomedical Sciences and Public Health, Polytechnic University of Marche, Ancona, Italy.

出版信息

Antimicrob Agents Chemother. 2012 Nov;56(11):5994-7. doi: 10.1128/AAC.01487-12. Epub 2012 Aug 13.

Abstract

The macrolide-aminoglycoside-streptothricin (MAS) element, an ∼4.2-kb insertion containing erm(B) and aphA3 resistance determinants, distinguishes Streptococcus pneumoniae transposon Tn1545/Tn6003 from Tn6002. Here, it is shown to be an unstable genetic element that, although it lacks recombinase genes, can exploit long, erm(B)-containing direct repeats acting as att sites for spontaneous excision that may result in loss. Consequent to excision, which is RecA independent, Tn1545/Tn6003 changes to Tn6002. In pneumococcal populations harboring Tn1545/Tn6003, the latter appears to coexist with Tn6002.

摘要

大环内酯-氨基糖苷-链霉菌素(MAS)元件是一个约 4.2kb 的插入片段,包含 erm(B)和 aphA3 耐药决定因子,可将肺炎链球菌转座子 Tn1545/Tn6003 与 Tn6002 区分开来。本文显示该元件是一个不稳定的遗传元件,尽管它缺乏重组酶基因,但可以利用长 erm(B) 内含子直接重复序列作为 att 位点,进行自发缺失,这可能导致 erm(B)的丢失。缺失是 RecA 非依赖性的,随后 Tn1545/Tn6003 转变成 Tn6002。在携带 Tn1545/Tn6003 的肺炎链球菌群体中,后者似乎与 Tn6002 共存。

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