Abstract
Listeria monocytogenes is a Gram‐positive, intracellular pathogen harboring the surface‐associated virulence factor InlB, which enables entry into certain host cells. Structurally diverse wall teichoic acids (WTAs), which can also be differentially glycosylated, determine the antigenic basis of the various Listeria serovars. WTAs have many physiological functions; they can serve as receptors for bacteriophages, and provide a substrate for binding of surface proteins such as InlB. In contrast, the membrane‐anchored lipoteichoic acids (LTAs) do not show significant variation and do not contribute to serovar determination. It was previously demonstrated that surface‐associated InlB non‐covalently adheres to both WTA and LTA, mediating its retention on the cell wall. Here, we demonstrate that in a highly virulent serovar 4b strain, two genes gtlB and gttB are responsible for galactosylation of LTA and WTA respectively. We evaluated the InlB surface retention in mutants lacking each of these two genes, and found that only galactosylated WTA is required for InlB surface presentation and function, cellular invasiveness and phage adsorption, while galactosylated LTA plays no role thereof. Our findings demonstrate that a simple pathogen‐defining serovar antigen, that mediates bacteriophage susceptibility, is necessary and sufficient to sustain the function of an important virulence factor.
Highlights
Listeria monocytogenes is a Gram-positive, facultative intracellular pathogen, causing listeriosis, a foodborne infectious disease with a significant global burden (de Noordhout et al, 2014)
The data presented here demonstrate that wall teichoic acids (WTAs), but not lipoteichoic acids (LTAs), is the primary mediator of Internalin B (InlB) surface retention and function
While we did not observe any recognizable difference in growth rate between the wild-type strain and the gtlB or gttB mutants (Supplementary Figure S2), we found that cellular invasiveness is impaired only in the galactose-deficient WTA mutant, due to loss of InlB
Summary
Listeria monocytogenes is a Gram-positive, facultative intracellular pathogen, causing listeriosis, a foodborne infectious disease with a significant global burden (de Noordhout et al, 2014). A significant decrease in cell-associated InlB was observed in the 1042ΔgttB mutant, with a concomitant increase of InlB secreted into the supernatant (Figure 3a) This loss of InlB surface localization was equivalent to that in the gttA mutant (Supplementary Figure S1), which mediates galactosylation of both WTA and LTA (Sumrall et al, 2019).This phenotype was complemented by expressing gttB from an integrative plasmid (Monk, Gahan, & Hill, 2008), InlB did not return entirely to WT levels, likely due to incomplete complementation (Figure 3a). InlA surface expression (Sumrall et al, 2019) is unaffected by the galactosylation of both LTA and WTA in this strain, meaning the invasion reduction observed here is mainly mediated by loss of InlB retention Together, these data highlight that Gal-WTA alone is necessary and sufficient to retain and display InlB at the cell surface, and that GalLTA does not play a measurable role in presenting of InlB
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
