Abstract
Pathoadaptive mutations linked to c-di-GMP signalling were investigated in neonatal meningitis-causing Escherichia coli (NMEC). The results indicated that NMEC strains deficient in RpoS (the global stress regulator) maintained remarkably low levels of c-di-GMP, a major bacterial sessility-motility switch. Deletion of ycgG2, shown here to encode a YcgG allozyme with c-di-GMP phosphodiesterase activity, and the restoration of RpoS led to a decrease in S-fimbriae, robustly produced in artificial urine, hinting that the urinary tract could serve as a habitat for NMEC. We showed that NMEC were skilled in aerobic citrate utilization in the presence of glucose, a property that normally does not exist in E. coli. Our data suggest that this metabolic novelty is a property of extraintestinal pathogenic E. coli since we reconstituted this ability in E. coli UTI89 (a cystitis isolate) via deactivation rpoS; additionally, a set of pyelonephritis E. coli isolates were shown here to aerobically use citrate in the presence of glucose. We found that the main reason for this metabolic capability is RpoS inactivation leading to the production of the citrate transporter CitT, exploited by NMEC for ferric citrate uptake dependent on YcgG2 (an allozyme with c-di-GMP phosphodiesterase activity).
Highlights
IntroductionThe adaptive potential to abiotic stress of different E. coli groups defines their ability to thrive in restrictive niches
Along with metabolic plasticity, the adaptive potential to abiotic stress of different E. coli groups defines their ability to thrive in restrictive niches
With the aim to investigate the role of c-di-GMP signalling in the lifestyle of neonatal meningitiscausing Escherichia coli (NMEC), we measured the total c-di-GMP levels extracted from bacterial colonies produced by different extraintestinal pathogenic E. coli (ExPEC) strains compared to levels produced by the commensal E. coli MG1655 (Fig. 1a)
Summary
The adaptive potential to abiotic stress of different E. coli groups defines their ability to thrive in restrictive niches. There are two groups of NMEC strains, those with active (e.g., E. coli C5) and inactive (e.g., E. coli IHE3034 and RS218) RpoS29, and the potential evolutionary reason underlying RpoS inactivation and the impact of this metabolic adaptation is an interest of this study. Another type of gene alteration gives rise to new allelic variants that may result in active gene products. The versatile lifestyle of ExPEC variants prompted us to investigate the role of c-di-GMP and RpoS in the pathoadaptation of NMEC and other ExPEC strains
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