Inter-species horizontal transfer resulting in core-genome and niche-adaptive variation within Helicobacter pylori.
BACKGROUND
Horizontal gene transfer is central to evolution in most bacterial species. The detection of exchanged regions is often based upon analysis of compositional characteristics and their comparison to the organism as a whole. In this study we describe a new methodology combining aspects of established signature analysis with textual analysis approaches. This approach has been used to analyze the two available genome sequences of H. pylori.


RESULTS
This gene-by-gene analysis reveals a wide range of genes related to both virulence behaviour and the strain differences that have been relatively recently acquired from other sequence backgrounds. These frequently involve single genes or small numbers of genes that are not associated with transposases or bacteriophage genes, nor with inverted repeats typically used as markers for horizontal transfer. In addition, clear examples of horizontal exchange in genes associated with 'core' metabolic functions were identified, supported by differences between the sequenced strains, including: ftsK, xerD and polA. In some cases it was possible to determine which strain represented the 'parent' and 'altered' states for insertion-deletion events. Different signature component lengths showed different sensitivities for the detection of some horizontally transferred genes, which may reflect different amelioration rates of sequence components.


CONCLUSIONS
New implementations of signature analysis that can be applied on a gene-by-gene basis for the identification of horizontally acquired sequences are described. These findings highlight the central role of the availability of homologous substrates in evolution mediated by horizontal exchange, and suggest that some components of the supposedly stable 'core genome' may actually be favoured targets for integration of foreign sequences because of their degree of conservation.
Saunders
Nigel J
NJ
Bacterial Pathogenesis and Functional Genomics Group, The Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, UK. Nigel.Saunders@path.ox.ac.uk
Boonmee
Prawit
P
Peden
John F
JF
Jarvis
Stephen A
SA
D000222:Adaptation, Physiological; D001435:Bacteriophages / Q000378:metabolism; D017124:Conserved Sequence; D004258:DNA Polymerase III / Q000378:metabolism; D029968:Escherichia coli Proteins / Q000378:metabolism; D019143:Evolution, Molecular; D017353:Gene Deletion; D005786:Gene Expression Regulation; D022761:Gene Transfer, Horizontal; D005798:Genes, Bacterial; D014644:Genetic Variation; D016678:Genome; D016680:Genome, Bacterial; D016480:Helicobacter pylori / Q000235:genetics* / Q000378:metabolism; D019426:Integrases / Q000378:metabolism; D008565:Membrane Proteins / Q000378:metabolism; D008957:Models, Genetic; D015233:Models, Statistical; D008969:Molecular Sequence Data; D016366:Open Reading Frames; D017434:Protein Structure, Tertiary; D017422:Sequence Analysis, DNA; D013045:Species Specificity; D014774:Virulence
D029968:Escherichia coli Proteins; C096452:FtsK protein, E coli; D008565:Membrane Proteins; C065639:DNA polymerase A; D019426:Integrases; C473361:XerD protein, E coli; D004258:DNA Polymerase III