Abstract
A genetic screen for colonization factors of the human stomach pathogen Helicobacter pylori took a surprising turn with the discovery that some colonization mutants had lost helical cell morphology. Further pursuit of direct morphology screens revealed a large H. pylori 'shapesome' complex consisting of peptidoglycan modification and precursor synthesis enzymes, a cytoskeletal element and putative scaffold or regulatory proteins that promote enhanced asymmetric cell wall growth. Functional characterization of H. pylori shape mutants indicates multiple roles for cell shape during colonization of mucosal surfaces. Conservation of both the molecular constituents of the H. pylori cell shape program and a newly appreciated enrichment of this morphotype at mucosal surface suggests that helical organisms may be particularly well poised to exploit host perturbations to become pathogens.