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

被引:11
作者
Kim, Moonjeong [1 ,2 ]
Kim, Minji [2 ]
Kim, Kwang-sun [1 ,2 ]
机构
[1] Pusan Natl Univ, Dept Chem, Busan 46241, South Korea
[2] Pusan Natl Univ, Chem Inst Funct Mat, Busan 46241, South Korea
基金
新加坡国家研究基金会;
关键词
Ribonuclease III; YmdB; Biofilm formation; Antibiotic resistance; SucA; Trans-acting regulator; RNASE-III; ANTIBIOTIC-RESISTANCE; BACTERIAL BIOFILMS; GENETIC-ANALYSIS; MESSENGER-RNA;
D O I
10.1016/j.bbrc.2016.12.157
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 YmdBlike 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 multidrugresistant bacteria. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码:252 / 257
页数:6
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