鲍曼不动杆菌氟喹诺酮类耐药的新机制。
Novel mechanism for fluoroquinolone resistance in Acinetobacter baumannii.
机构信息
Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, USA.
出版信息
Antimicrob Agents Chemother. 2012 Sep;56(9):4955-7. doi: 10.1128/AAC.00739-12. Epub 2012 Jun 25.
Abstract
An EZ::TN<R6Kγori/KAN-2>Tnp transposon insertion in an open reading frame of unknown function (ncr) in Acinetobacter baumannii resulted in an 8-fold increase in ciprofloxacin resistance (Cip(r)). Transposon insertions in an ncr mutant that reduced Cip(r) back to wild type mapped to three genes encoding subunits of the RecCBD exonuclease. The ncr mutation increased transcription of the recCBD genes, and overexpression of the recCBD genes in a wild-type background resulted in a 4-fold increase in Cip(r).
摘要
在鲍曼不动杆菌中，一个 EZ::TN<R6Kγori/KAN-2>Tnp 转座子插入到一个未知功能的开放阅读框（ncr）中，导致对环丙沙星的耐药性增加了 8 倍（Cip(r)）。在降低 Cip(r)回到野生型的 ncr 突变体中，转座子插入位于三个编码 RecCBD 外切酶亚基的基因上。ncr 突变增加了 recCBD 基因的转录，在野生型背景下过表达 recCBD 基因导致 Cip(r)增加了 4 倍。
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