Abstract
Helical cell shape is necessary for efficient stomach colonization by Helicobacter pylori, but the molecular mechanisms for generating helical shape remain unclear. The helical centerline pitch and radius of wild-type H. pylori cells dictate surface curvatures of considerably higher positive and negative Gaussian curvatures than those present in straight- or curved-rod H. pylori. Quantitative 3D microscopy analysis of short pulses with either N-acetylmuramic acid or D-alanine metabolic probes showed that cell wall growth is enhanced at both sidewall curvature extremes. Immunofluorescence revealed MreB is most abundant at negative Gaussian curvature, while the bactofilin CcmA is most abundant at positive Gaussian curvature. Strains expressing CcmA variants with altered polymerization properties lose helical shape and associated positive Gaussian curvatures. We thus propose a model where CcmA and MreB promote PG synthesis at positive and negative Gaussian curvatures, respectively, and that this patterning is one mechanism necessary for maintaining helical shape.
Highlights
Helicobacter pylori is a helical Gram-negative bacterium that colonizes the human stomach and can cause stomach ulcers and gastric cancers (Correa, 1988)
Using superresolution microscopy and 3D quantitative image analysis, we show that synthesis is enhanced at negative Gaussian curvature as well as at a limited range of positive Gaussian curvatures
77 CcmA is enriched at the window of positive Gaussian curvatures where enhanced synthesis is observed. We propose that both MreB and CcmA help recruit PG synthesis activity locally and that PG synthesis patterning is one mechanism that plays a fundamental role in helical cell shape maintenance
Summary
Helicobacter pylori is a helical Gram-negative bacterium that colonizes the human stomach and can cause stomach ulcers and gastric cancers (Correa, 1988). Helical cell shape is necessary for efficient stomach colonization (Bonis et al, 2010; Sycuro et al, 2012, 2010), underscoring its importance. Non-essential contributors to cell shape have been identified, but the question of how they 42 enable H. pylori to be helical remains largely unsolved. As is the case for most bacteria (Höltje, 1998), the structure of the H. pylori peptidoglycan (PG) cell wall (sacculus) is responsible for the shape of the cell; purified cell walls maintain helical shape (Sycuro et al, 2010). Crosslinked PG strands form the cell wall, a large mesh-like macromolecule that surrounds the cell and counteracts the cell’s turgor pressure (Höltje, 1998; Typas et al., 2012). The PG monomer is synthesized in the cytoplasm and subsequently flipped across the inner membrane and incorporated into the existing PG by the glycosyltransferase activities of penicillin binding proteins (PBPs) and perhaps shape, elongation, division and sporulation (SEDS) proteins and the transpeptidation activities of PBPs (Meeske et al, 2016; Sauvage et al, 2008)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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.
