Skip to main content
ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #324879

Research Project: PREVENTION AND CHARACTERIZATION OF PERSISTENT COLONIZATION BY E. COLI O157:H7 AND OTHER SHIGA TOXIN-PRODUCING E. COLI (STEC) IN CATTLE

Location: Food Safety and Enteric Pathogens Research

Title: Implications of down regulation of rcsA and rcsA-regulated colanic acid biosynthesis genes in increased acid sensitivity and enhanced curli and biofilm production in enterohemorrhagic Escherichia coli O157:H7

Author
item Sharma, Vijay

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 2/29/2016
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Enterohemorrhagic Escherichia coli (E. coli) O157:H7 strain 86-24, originally linked to a disease outbreak in the western USA in 1982, exhibits acid resistance as indicated by its ability to survive exposure to acidic conditions (pH2.5) for several hours. The strain 86-24 is a poor biofilm producer which correlates with the production of low levels of curli fimbriae as assessed by Congo red binding assays, electron microscopy, and the levels of curlin (major structural protein of curli) expression using Western blotting. This parental strain 86-24, however, can produce variants that are highly acid sensitive but show increased biofilm formation and enhanced Congo red binding (CR plus), the latter correlating with increased curli expression. Transcriptomic analysis of the CR plus variant revealed significantly reduced expression of genes associated with acid resistance, colanic acid production, but enhanced expression of genes encoding flagellar motility compared to the low Congo red binding (CR negative) parental strain. The expression of rcsA, which encodes a positive regulator (RcsA) of genes for colanic acid biosynthesis, was highly down regulated in the CR plus variant. RcsA has been shown to serve as an auxiliary to the RcsB of the Rcs phosphorelay system in controlling colanic acid biosynthesis and expression of genes governing flagellar motility. In this study, we demonstrated that while rcsA was required for colanic acid biosynthesis and flagellar motility, findings that are in agreement with the other published reports, the rcsA gene did not negate the high levels of curli expression and biofilm formation in the CR plus variant. RcsB reportedly regulates the expression of acid resistance in E. coli by interacting with GadE, which is the major regulator of genes required for the high level acid resistance. Whether RcsA has any role in controlling acid resistance through cooperation with RcsB or some other factors is not yet fully understood.