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YmdB介导的sucA下调抑制大肠杆菌生物膜形成并诱导对阿泊拉霉素敏感。

YmdB-mediated down-regulation of sucA inhibits biofilm formation and induces apramycin susceptibility in Escherichia coli.

作者信息

Kim Moonjeong, Kim Minji, Kim Kwang-Sun

机构信息

Department of Chemistry and Chemistry Institute of Functional Materials, Pusan National University, Busan, 46241, South Korea.

Chemistry Institute for Functional Materials, Pusan National University, Busan, 46241, South Korea.

出版信息

Biochem Biophys Res Commun. 2017 Jan 29;483(1):252-257. doi: 10.1016/j.bbrc.2016.12.157. Epub 2016 Dec 26.

DOI:10.1016/j.bbrc.2016.12.157
PMID:28034758
Abstract

Antibiotic resistance associated with biofilm formation is a major concern when treating bacterial infections with drugs. The genes and pathways involved in biofilm formation have been extensively studied and are also involved in antibiotic resistance. Recent studies show that overexpression of Escherichia coli (E. coli) YmdB protein alters gene expression profiles and inhibits biofilm formation. Therefore, it is expected that YmdB and its regulated genes play a key role in development of biofilm and antibiotic resistance phenotypes. The present study screened antibiotics to identify those whose susceptibility profiles were regulated by YmdB levels. This protocol identified apramycin. Additional screening for genes negatively regulated by inactivation of RNase III activity via YmdB overexpression revealed that a gene associated with the tricarboxylic acid cycle gene, sucA, was necessary for the YmdB-like phenotype. Taken together, these data suggest that regulation of RNase III activity by trans-acting factors may be the key to identifying genes or pathways connecting biofilm and antibiotic resistance phenotypes. This information could be used to reduce the emergence of biofilm-associated multidrug-resistant bacteria.

摘要

在使用药物治疗细菌感染时,与生物膜形成相关的抗生素耐药性是一个主要问题。参与生物膜形成的基因和途径已得到广泛研究,并且也与抗生素耐药性有关。最近的研究表明,大肠杆菌(E. coli)YmdB蛋白的过表达会改变基因表达谱并抑制生物膜形成。因此,预计YmdB及其调控基因在生物膜和抗生素耐药表型的发展中起关键作用。本研究筛选了抗生素,以确定那些敏感性谱受YmdB水平调控的抗生素。该方案鉴定出了安普霉素。通过YmdB过表达对因核糖核酸酶III活性失活而负调控的基因进行的额外筛选表明,与三羧酸循环基因sucA相关的一个基因对于YmdB样表型是必需的。综上所述,这些数据表明反式作用因子对核糖核酸酶III活性的调控可能是识别连接生物膜和抗生素耐药表型的基因或途径的关键。这些信息可用于减少生物膜相关多重耐药细菌的出现。

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