Publications by authors named "Tate Sessler"

Evident in its name, the gastric pathogen has a helical cell morphology which facilitates efficient colonization of the human stomach. An improved light-focusing strategy allowed us to robustly distinguish even subtle perturbations of cell morphology by deviations in light-scattering properties measured by flow cytometry. Profiling of an arrayed genome-wide deletion library identified 28 genes that influence different aspects of cell shape, including properties of the helix, cell length or width, cell filament formation, cell shape heterogeneity, and cell branching.

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The helical cell shape of Helicobacter pylori is highly conserved and contributes to its ability to swim through and colonize the viscous gastric mucus layer. A multi-faceted peptidoglycan (PG) modification programme involving four recently characterized peptidases and two accessory proteins is essential for maintaining H. pylori's helicity.

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Animal models are important tools for studies of human disease, but developing these models is a particular challenge with regard to organisms with restricted host ranges, such as the human stomach pathogen Helicobacter pylori. In most cases, H. pylori infects the stomach for many decades before symptoms appear, distinguishing it from many bacterial pathogens that cause acute infection.

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Article Synopsis
  • All organisms have mechanisms to repair their DNA, which is crucial for their survival and the survival of their offspring; these mechanisms can also lead to genetic diversity.
  • Sequencing of bacteria has shown significant genetic variation even within the same species, emphasizing the need to understand how DNA recombination and repair work.
  • Helicobacter pylori, a pathogen that infects the human stomach, is a valuable model for studying these processes due to its capacity for genetic diversification through recombination and repair pathways.
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