Abstract
Pseudomonas aeruginosa, a major cause of nosocomial infection, can survive under diverse environmental conditions. Its great adaptive ability is dependent on its multiple signaling systems such as the two-component system (TCS). A TCS FleS/FleR has been previously identified to positively regulate a variety of virulence-related traits in P. aeruginosa PAO1 including motility and biofilm formation which are involved in the acute and chronic infections, respectively. However, the molecular mechanisms underlying these regulations are still unclear. In this study, we first analyzed the regulatory roles of each domains in FleS/FleR and characterized key residues in the FleS-HisKA, FleR-REC and FleR-AAA domains that are essential for the signaling. Next, we revealed that FleS/FleR regulates biofilm formation in a c-di-GMP and FleQ dependent manner. Lastly, we demonstrated that FleR can regulate flagellum biosynthesis independently without FleS, which explains the discrepant regulation of swimming motility by FleS and FleR.
Highlights
Pseudomonas aeruginosa is an opportunistic Gram-negative pathogen that causes a variety of acute and chronic infections in humans (Driscoll et al, 2007; Coggan and Wolfgang, 2012)
In addition to control swarming motility (Kollaran et al, 2019), our recent study has demonstrated that the two-component system (TCS) FleS/FleR is involved in the regulation of biofilm formation and swimming motility in P. aeruginosa PAO1 (Zhou et al, 2021)
Unlike typical histidine kinases which contain a transmembrane domain, FleS only consists of three domains namely PAS, HisKA (HK), and HATPase (HA) (Figure 1A)
Summary
Pseudomonas aeruginosa is an opportunistic Gram-negative pathogen that causes a variety of acute and chronic infections in humans (Driscoll et al, 2007; Coggan and Wolfgang, 2012). P. aeruginosa has an unusually large genome size of 6.4 Mbp with nearly 6,000 genes including a majority of them encoding proteins associated with virulence factors, secretion systems, motility, efflux pumps, chemotaxis and biofilm formation, conferring to the pathogen great ability to infect and adapt to diverse host habitats (Silby et al, 2011; Cao et al, 2017) It is highly mobile and armed with full virulence factors to establish colonization at the early acute infection gradually shifts to an adapted situation with increased persistence and biofilm formation if not successfully eradicated by the human immune system (Sousa and Pereira, 2014). This pathogen can survive and thrive in diverse terrestrial and aquatic niches with its unique ability in sensing and responding to environmental changes (Rahme et al, 1995).
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