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Chapter 3 : Genomic Fluidity of the Human Gastric Pathogen

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Abstract:

Genomic fluidity associated with has important consequences for clinical management of the gastroduodenal diseases caused by colonization with this significant pathogen. This chapter discusses the attributes of the genomes of different strains and the roles of strain-specific genes from the genomic plasticity region. Researchers analyze two core genome data sets, one at the genus level and the other at the species level. genomes were compared at the biochemical level, based on the presence of enzymes in their metabolic pathway. The genome was found to be subdivided into two clades, highlighting the fact that they have two distinct modes of biochemical transformation. It would be very interesting if such varied metabolic repertoires indeed represent genomic fluidity across these two clades. In , three types of genomic islands coding for the type IV secretion system were identified: (i) the cytotoxin-associated gene pathogenicity island (cagPAI), (ii) the competence island (comB gene cluster), and (iii) the plasticity zone. Geneticists think that the transformation apparatus has evolved conservatively in and is typically present in all the strains. This conservation explains why genomic fluidity in is so common, especially when the deletions and rearrangements due to natural transformation and transposition are described as frequently occurring phenomena. -induced chronic gastritis is a definitive risk factor for the development of gastric cancer.

Citation: Ahmed N, Devi S, Tenguria S, Majid M, Rahman S, Hasnain S. 2012. Genomic Fluidity of the Human Gastric Pathogen , p 27-43. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch3
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FIGURE 1

Schema showing the origins of genetic heterogeneity among bacteria and its implications. The genetic diversity among microbial pathogens is possibly due to the acquisition or loss of DNA. Mechanisms such as mutation, transformation, recombination, transposition, transduction, and horizontal gene transfer, and genetic elements such as genomic or pathogenic islands, plasmids, etc., result in DNA rearrangements, inversions, duplications, deletions, and insertions that lead to alteration of gene expression and to loss or gain of gene function. These alterations in the genome are responsible for novel phenotypes, varied drug resistance, enhanced pathogenicity, and bacterial fitness in diverse environments.doi:10.1128/9781555817213.ch03f01

Citation: Ahmed N, Devi S, Tenguria S, Majid M, Rahman S, Hasnain S. 2012. Genomic Fluidity of the Human Gastric Pathogen , p 27-43. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch3
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FIGURE 2

Orthologous genes of helicobacters (common gene pools): Every area in the Venn diagram represents a subset of the compared genomes and is labeled with the number of genes in the concerned subset. shares about 774 genes at the genome level, and shares about 1,244 genes, indicating closer connections at species level with conserved functions of genes. The core genome plateaus around ~1,244 genes with conserved functions, wherein horizontal gene transfer and positive selection are playing key roles in the adaptive evolution of this core genome.doi:10.1128/9781555817213.ch03f02

Citation: Ahmed N, Devi S, Tenguria S, Majid M, Rahman S, Hasnain S. 2012. Genomic Fluidity of the Human Gastric Pathogen , p 27-43. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch3
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FIGURE 3

Dendrogram based on comparative metabolomics of (produced by using KEGG). Organisms which share a larger number of enzymes are clustered together. This highlights the commonality of biochemical transformation between their metabolic pathways.doi:10.1128/9781555817213.ch03f03

Citation: Ahmed N, Devi S, Tenguria S, Majid M, Rahman S, Hasnain S. 2012. Genomic Fluidity of the Human Gastric Pathogen , p 27-43. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch3
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FIGURE 4

Acquisition of virulence, optimization of fitness, and geographically compartmentalized spread of (sub)populations ( ). Horizontal gene transfer and genome plasticity probably contributed to the evolution of pathogenic variants from nonpathogenic colonizers. Modern populations thus derived their gene pools from ancestral populations that arose on different continents and can be correlated with different migrations of human populations and other Neolithic events such as the arrival of agriculture. The beginning of agriculture and the domestication of farm animals (which seem to have occurred hand in hand but across multiple domestication events in a continent-specific manner) suggest a scenario, as depicted here, which can be linked to the acquisition of virulence by . It can be hypothesized that early bacterial communities originating from crop plants, animals, or rodent pests, etc., very common in the vicinity of early human societies, may have served as donors of some of the virulence gene cassettes. Such genetic elements may have been acquired by either bit by bit or en bloc, at some time, through horizontal gene transfer events. There is indirect evidence to this effect in the form of sequence and structural similarities of some of the virulence genes to their homologues in plant pathogens and environmental bacteria. Also, we think that the extraneous virulence genes may have conferred some survival advantage upon strains, making them fitter in different human and animal hosts and, as a result, the pathogen may have spread selectively in a geographically compartmentalized manner.doi:10.1128/9781555817213.ch03f04

Citation: Ahmed N, Devi S, Tenguria S, Majid M, Rahman S, Hasnain S. 2012. Genomic Fluidity of the Human Gastric Pathogen , p 27-43. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch3
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FIGURE 5

Arrangement of ORFs under different types of plasticity zone-encoded transposable elements (TnPZs) in (from ). Different regions/ORFs of the TnPZs have been color coded as per the conventions detailed by .doi:10.1128/9781555817213.ch03f05

Citation: Ahmed N, Devi S, Tenguria S, Majid M, Rahman S, Hasnain S. 2012. Genomic Fluidity of the Human Gastric Pathogen , p 27-43. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch3
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Tables

Generic image for table
TABLE 1

Features of the genomes

Citation: Ahmed N, Devi S, Tenguria S, Majid M, Rahman S, Hasnain S. 2012. Genomic Fluidity of the Human Gastric Pathogen , p 27-43. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch3
Generic image for table
TABLE 2

Distribution of plasticity zones in the genomes of different strains

Citation: Ahmed N, Devi S, Tenguria S, Majid M, Rahman S, Hasnain S. 2012. Genomic Fluidity of the Human Gastric Pathogen , p 27-43. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch3
Generic image for table
TABLE 3

Functional ORFs and homologies of the members of the plasticity region

Citation: Ahmed N, Devi S, Tenguria S, Majid M, Rahman S, Hasnain S. 2012. Genomic Fluidity of the Human Gastric Pathogen , p 27-43. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch3
Generic image for table
TABLE 4

Exploitation of genomic fluidity of for diagnostic and health care applications

Citation: Ahmed N, Devi S, Tenguria S, Majid M, Rahman S, Hasnain S. 2012. Genomic Fluidity of the Human Gastric Pathogen , p 27-43. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch3

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