The transcriptional antiterminator RfaH represses biofilm formation in Escherichia coli
The transcriptional antiterminator RfaH represses biofilm formation in Escherichia coli
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DOI：
10.1128/jb.188.4.1316-1331.2006
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发表时间：
2006-02-01
影响因子：
3.2
通讯作者：
Dobrindt, U
中科院分区：
文献类型：
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作者：
Beloin, C;Michaelis, K;Dobrindt, U
我们研究了调节和致病岛相关因子(HHA、rpos、LuxS、EVGA、RfaH和tRNA(5)(Leu))对尿路致病性大肠杆菌(UPEC)536株生物被膜形成的影响。只有编码转录抗终止子的rfaH失活才能增加E.coli536的初始黏附和生物膜形成。在非致病性大肠杆菌K-12分离株MG1655中，rfaH失活导致相同的表型。对野生型毒株536和该毒株的rfaH突变体的转录组分析表明，rfaH的缺失与流感同源基因的表达增加有关。流感编码抗原43(Ag43)，它介导自我聚集和生物膜的形成。我们证实，RJAH的缺失会导致大肠杆菌K-12和UPEC中流感和流感样转录本水平的增加。支持RfaH通过降低Ag43水平抑制生物膜形成的假设，大肠杆菌MG1655rfaH的生物膜增加表型在Flu灭活后被逆转。然而，两个流感同源基因的删除并没有改变突变的536rfaH的行为。我们的结果表明，MG1655rfaH菌株强大的初始黏附和生物被膜形成能力是由Ag43稳态产量的增加和可能由于依赖于rfaH的内毒素耗尽而增加的Ag43提呈所介导的。尽管在UPEC株536和K-12株MG1655中，rfaH在生物膜表型中的作用不同，但本研究表明，rfaH除了影响细菌毒力因子的表达外，还负向控制Ag43的表达和表面提呈，可能还有另一种介导细胞-细胞相互作用和生物膜形成的Ag43非依赖因子(S)。
We investigated the influence of regulatory and pathogenicity island-associated factors (Hha, RpoS, LuxS, EvgA, RfaH, and tRNA(5)(Leu)) on biofilm formation by uropathogenic Escherichia coli (UPEC) strain 536. Only inactivation of rfaH, which encodes a transcriptional antiterminator, resulted in increased initial adhesion and biofilm formation by E. coli 536. rfaH inactivation in nonpathogenic E. coli K-12 isolate MG1655 resulted in the same phenotype. Transcriptome analysis of wild-type strain 536 and an rfaH mutant of this strain revealed that deletion of rfaH correlated with increased expression of flu orthologs. flu encodes antigen 43 (Ag43), which mediates autoaggregation and biofilm formation. We confirmed that deletion of rjaH leads to increased levels of flu and flu-like transcripts in E. coli K-12 and UPEC. Supporting the hypothesis that RfaH represses biofilm formation through reduction of the Ag43 level, the increased-biofilm phenotype of E. coli MG1655rfaH was reversed upon inactivation of flu. Deletion of the two flu orthologs, however, did not modify the behavior of mutant 536rfaH. Our results demonstrate that the strong initial adhesion and biofilm formation capacities of strain MG1655rfaH are mediated by both increased steady-state production of Ag43 and likely increased Ag43 presentation due to null rfaH-dependent lipopolysaccharide depletion. Although the roles of rfaH in the biofilm phenotype are different in UPEC strain 536 and K-12 strain MG1655, this study shows that RfaH, in addition to affecting the expression of bacterial virulence factors, also negatively controls expression and surface presentation of Ag43 and possibly another Ag43-independent factor(s) that mediates cell-cell interactions and biofilm formation.