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Pathogenicity of the human pathogen  Helicobacter pylori  relies upon its capacity to adapt to a hostile environment and to escape from the host response. Therefore, cell shape, motility, and pH homeostasis of these bacteria are specifically adapted to the gastric mucus. We have found that the helical shape of  H. pylori  depends on  c oiled  c oil  r ich  p roteins (Ccrp), which form extended filamentous structures  in vitro  and  in vivo , and are differentially required for the maintenance of cell morphology. We have developed an  in vivo  localization system for this pathogen. Consistent with a cytoskeleton-like structure, Ccrp proteins localized in a regular punctuate and static pattern within  H. pylori  cells. Ccrp genes show a high degree of sequence variation, which could be the reason for the morphological diversity between  H. pylori  strains. In contrast to other bacteria, the actin-like MreB protein is dispensable for viability in  H. pylori , and does not affect cell shape, but cell length and chromosome segregation. In addition,  mreB  mutant cells displayed significantly reduced urease activity, and thus compromise a major pathogenicity factor of  H. pylori . Our findings reveal that Ccrp proteins, but not MreB, affect cell morphology, while both cytoskeletal components affect the development of pathogenicity factors and/or cell cycle progression.

A Novel System of Cytoskeletal Elements in the Human Pathogen Helicobacter pylori