Qnr 对质粒拓扑异构酶 Gyrase 毒素 CcdB 和 ParE 的影响。
Effect of Qnr on Plasmid Gyrase Toxins CcdB and ParE.
机构信息
Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, USA Inje University College of Medicine, Busan, South Korea.
Lahey Hospital and Medical Center, Burlington, Massachusetts, USA
出版信息
Antimicrob Agents Chemother. 2015 Aug;59(8):5078-9. doi: 10.1128/AAC.00524-15. Epub 2015 Jun 8.
Abstract
Plasmid toxins CcdB and ParE are part of addiction systems promoting plasmid maintenance. Both target host DNA gyrase, as do quinolones and plasmid-determined Qnr proteins that protect gyrase from quinolone inhibition. We cloned qnrB4, qnrS1, ccdB, parE, and the antitoxin-encoding genes ccdA and parD on compatible plasmids and tested them in combination. CcdB and ParE had no specific effect on quinolone susceptibility or Qnr protection, and Qnr did not act as a CcdB or ParE antitoxin.
摘要
质粒毒素 CcdB 和 ParE 是促进质粒维持的成瘾系统的一部分。两者都靶向宿主 DNA 回旋酶，就像喹诺酮类药物和质粒决定的 Qnr 蛋白一样，它们可以保护回旋酶免受喹诺酮类药物的抑制。我们将 qnrB4、qnrS1、ccdB、parE 以及抗毒素编码基因 ccdA 和 parD 克隆到相容质粒上，并对它们进行了组合测试。CcdB 和 ParE 对喹诺酮类药物的敏感性或 Qnr 保护没有特异性作用，而 Qnr 也不作为 CcdB 或 ParE 的抗毒素。
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