Role of SdiA on Biofilm Formation by Atypical Enteropathogenic Escherichia coli

Abstract

Atypical enteropathogenic Escherichia coli are capable to form biofilm on biotic and abiotic surfaces, regardless of the adherence pattern displayed. Several E. coli mechanisms are regulated by Quorum sensing (QS), including virulence factors and biofilm formation. Quorum sensing is a signaling system that confers bacteria with the ability to respond to chemical molecules known as autoinducers. Suppressor of division inhibitor (SdiA) is a QS receptor present in atypical enteropathogenic E. coli (aEPEC) that detects acyl homoserine lactone (AHL) type autoinducers. However, these bacteria do not encode an AHL synthase, but they are capable of sensing AHL molecules produced by other species, establishing an inter-species bacterial communication. In this study, we performed experiments to evaluate pellicle, ring-like structure and biofilm formation on wild type, sdiA mutants and complemented strains. We also evaluated the transcription of genes involved in different stages of biofilm formation, such as bcsA, csgA, csgD, fliC and fimA. The sdiA mutants were capable of forming thicker biofilm structures and showed increased motility when compared to wild type and complemented strains. Moreover, they also showed denser pellicles and ring-like structures. Quantitative real-time PCR (qRT-PCR) analysis demonstrated increased csgA, csgD and fliC transcription on mutant strains. Biofilm formation, as well as csgD, csgA and fimA transcription decreased on wild type strains by the addition of AHL. These results indicate that SdiA participates on the regulation of these phenotypes in aEPEC and that AHL addition enhances the repressor effect of this receptor on the transcription of biofilm and motility related genes.

SdiA, a Quorum-Sensing Regulator, Suppresses Fimbriae Expression, Biofilm Formation, and Quorum-Sensing Signaling Molecules Production in Klebsiella pneumoniae

“…Biofilm formation in the presence of exogenous AHL rendered distinct results: while no effect was observed for the mutant strain, the wild-type formed less biofilm. These results are in agreement with studies that reported an increase in biofilm formation and pellicle formation by E. coli sdiA mutant strains (Lee et al, 2007;Sharma et al, 2010;Culler et al, 2018). Similarly to our findings, these authors also noticed no change in biofilm formation by the mutant strain in the presence of AHL, whereas the wild-type strain has the formation of biofilm inhibited.…”

“…In many pathogens, the SdiA regulator modulates the expression of several virulence factors, such as adherence and motility ( Kanamaru et al, 2000 ; Sharma et al, 2010 ), multidrug resistance ( Tavio et al, 2010 ), biofilm formation ( Culler et al, 2018 ) and acid tolerance ( Ma et al, 2020 ). Concerning K. pneumoniae , little is known about the role of SdiA in the pathogenesis of this bacterium and, to date, no member of the SdiA regulon had been described in K. pneumoniae .…”

“…Acting as a transcriptional regulator, SdiA has been implicated in the regulation of several cellular processes including cell division ( Sitnikov et al, 1996 ) and in the expression of virulence factors such as antibiotic resistance, motility and biofilm formation ( Kanamaru et al, 2000 ; Sharma et al, 2010 ; Antunes et al, 2010 ; Tavio et al, 2010 ; Culler et al, 2018 ; Ma et al, 2020 ). Bacterial cell division relies on the ftsQAZ operon, which encodes the FtsQ, FtsA, and FtsZ proteins responsible for recruiting and assembling cell division machinery in the septum.…”

“…SdiA plays an important role during cell division because it acts as a positive regulator in the expression of ftsQAZ operon ( Wang et al, 1991 ), and in vitro assays confirmed DNA-binding activity of purified SdiA to the ftsQ promoter ( Shimada et al, 2014 ). Regarding virulence factors, SdiA regulates biofilm formation through regulation of fimbriae and curli genes ( Culler et al, 2018 ). Studies have shown that fimbriae play an important role during biofilm formation by K. pneumoniae ( Schroll et al, 2010 ; Alcántar-Curiel et al, 2013 ), but the role of SdiA in this process has not yet been addressed in this bacterium.…”

SdiA Improves the Acid Tolerance of E. coli by Regulating GadW and GadY Expression

“…Most recent publications about SdiA have reported its gene regulatory function (Dyszel et al, 2010;Nguyen et al, 2015;Sabag-Daigle et al, 2015). A few reports revealed the roles of SdiA in diverse biological processes (Smith et al, 2011), such as cell division (Sitnikov et al, 1996), antibiotic resistance (Yang et al, 2006;Tavío et al, 2010), virulence (Kanamaru et al, 2000), and biofilm formation (Culler et al, 2018). Here, gain-and loss-of-function studies showed that SdiA positively regulated mild and extreme acid (pH 3-6) tolerance ability of both E. coli strains SM10λpir and BW25113.…”