Quantum changes in Helicobacter pylori gene expression accompany host-adaptation.
Helicobacter pylori is a highly successful gastric pathogen. High genomic plasticity allows its adaptation to changing host environments. Complete genomes of H. pylori clinical isolate UM032 and its mice-adapted serial derivatives 298 and 299, generated using both PacBio RS and Illumina MiSeq sequencing technologies, were compared to identify novel elements responsible for host-adaptation. The acquisition of a jhp0562-like allele, which encodes for a galactosyltransferase, was identified in the mice-adapted strains. Our analysis implies a new β-1,4-galactosyltransferase role for this enzyme, essential for Ley antigen expression. Intragenomic recombination between babA and babB genes was also observed. Further, we expanded on the list of candidate genes whose expression patterns have been mediated by upstream homopolymer-length alterations to facilitate host adaption. Importantly, greater than four-fold reduction of mRNA levels was demonstrated in five genes. Among the down-regulated genes, three encode for outer membrane proteins, including BabA, BabB and HopD. As expected, a substantial reduction in BabA protein abundance was detected in mice-adapted strains 298 and 299 via Western analysis. Our results suggest that the expression of Ley antigen and reduced outer membrane protein expressions may facilitate H. pylori colonisation of mouse gastric epithelium.
The Marshall Centre for Infectious Diseases Research and Training, School of Pathology and Laboratory Medicine, The University of Western Australia, Nedlands, Western Australia, Australia.
Eng-Guan
EG
Chua
The Marshall Centre for Infectious Diseases Research and Training, School of Pathology and Laboratory Medicine, The University of Western Australia, Nedlands, Western Australia, Australia.|School of Computer Science and Software Engineering, The University of Western Australia, Australia.
Michael J
MJ
Wise
Department of Medical Microbiology, University of Malaya, Kuala Lumpur, Malaysia.
Yalda
Y
Khosravi
National Cancer Centre of Singapore, Singapore.
Shih-Wee
SW
Seow
National Cancer Centre of Singapore, Singapore.
Arlaine A
AA
Amoyo
Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, Sweden.|LKC School of Medicine, Nanyang Technological University, Singapore.|SCELSE Microbiome Centre, Nanyang Technological University, Singapore.
Sven
S
Pettersson
The Marshall Centre for Infectious Diseases Research and Training, School of Pathology and Laboratory Medicine, The University of Western Australia, Nedlands, Western Australia, Australia.
Fanny
F
Peters
The Marshall Centre for Infectious Diseases Research and Training, School of Pathology and Laboratory Medicine, The University of Western Australia, Nedlands, Western Australia, Australia.
Chin-Yen
CY
Tay
The Marshall Centre for Infectious Diseases Research and Training, School of Pathology and Laboratory Medicine, The University of Western Australia, Nedlands, Western Australia, Australia.
Timothy T
TT
Perkins
Department of Medical Microbiology, University of Malaya, Kuala Lumpur, Malaysia.
Mun-Fai
MF
Loke
The Marshall Centre for Infectious Diseases Research and Training, School of Pathology and Laboratory Medicine, The University of Western Australia, Nedlands, Western Australia, Australia.|UM Marshall Centre, High Impact Research Building, University of Malaya, 50603 Kuala Lumpur, Malaysia.
Barry J
BJ
Marshall
Department of Medical Microbiology, University of Malaya, Kuala Lumpur, Malaysia.
Jamuna
J
Vadivelu
D000222:Adaptation, Physiological; D000818:Animals; D015870:Gene Expression; D016680:Genome, Bacterial; D016480:Helicobacter pylori / Q000235:genetics* / Q000502:physiology; D054884:Host-Pathogen Interactions; D008070:Lipopolysaccharides / Q000096:biosynthesis; D051379:Mice; D009154:Mutation; D011789:Quantum Theory; D011995:Recombination, Genetic
D008070:Lipopolysaccharides
BabA; Helicobacter pylori; Lewis antigen; expression; host adaptation