Quantum changes in Helicobacter pylori gene expression accompany host-adaptation
Eng-Guan Chua1, Michael J Wise1,2, Yalda Khosravi3
1The Marshall Centre for Infectious Diseases Research and Training, School of Pathology and Laboratory Medicine, The University of Western Australia, Nedlands, Western Australia, Australia.
Helicobacter pylori adapted to mice by gaining a gene for Ley antigen expression and reducing outer membrane proteins like BabA. These changes likely aid its colonization of the mouse stomach.
Area of Science:
- Microbiology
- Genomics
- Pathogen Adaptation
Background:
- Helicobacter pylori is a successful gastric pathogen with high genomic plasticity.
- Understanding H. pylori adaptation mechanisms is crucial for controlling infections.
Purpose of the Study:
- To identify genetic elements enabling H. pylori adaptation to new host environments.
- To compare the genomes of a clinical isolate and its mouse-adapted derivatives.
Main Methods:
- Whole-genome sequencing using PacBio RS and Illumina MiSeq.
- Comparative genomic analysis of H. pylori strains.
- Analysis of gene expression and protein abundance.
Main Results:
- Mice-adapted strains acquired a jhp0562-like allele, encoding a β-1,4-galactosyltransferase essential for Ley antigen expression.
- Intragenomic recombination between babA and babB genes was observed.
- Down-regulation of genes, including outer membrane proteins BabA, BabB, and HopD, was demonstrated, correlating with reduced BabA protein abundance.
Conclusions:
- Acquisition of a galactosyltransferase for Ley antigen expression and reduced outer membrane protein expression may facilitate H. pylori colonization of the mouse gastric epithelium.
- Genomic plasticity, including gene acquisition and altered expression, is key to H. pylori host adaptation.
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