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The complete methylome of Helicobacter pylori UM032

The genome of the human gastric pathogen Helicobacter pylori encodes a large number of DNA methyltransferases (MTases), some of which are shared among many strains, and others of which are unique to a given strain. The MTases have potential roles in the survival of the bacterium. In this study, we s...

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Published in:BMC genomics 2015-06, Vol.16 (1), p.424-424, Article 424
Main Authors: Lee, Woon Ching, Anton, Brian P, Wang, Susana, Baybayan, Primo, Singh, Siddarth, Ashby, Meredith, Chua, Eng Guan, Tay, Chin Yen, Thirriot, Fanny, Loke, Mun Fai, Goh, Khean Lee, Marshall, Barry J, Roberts, Richard J, Vadivelu, Jamuna
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Language:English
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Summary:The genome of the human gastric pathogen Helicobacter pylori encodes a large number of DNA methyltransferases (MTases), some of which are shared among many strains, and others of which are unique to a given strain. The MTases have potential roles in the survival of the bacterium. In this study, we sequenced a Malaysian H. pylori clinical strain, designated UM032, by using a combination of PacBio Single Molecule, Real-Time (SMRT) and Illumina MiSeq next generation sequencing platforms, and used the SMRT data to characterize the set of methylated bases (the methylome). The N4-methylcytosine and N6-methyladenine modifications detected at single-base resolution using SMRT technology revealed 17 methylated sequence motifs corresponding to one Type I and 16 Type II restriction-modification (R-M) systems. Previously unassigned methylation motifs were now assigned to their respective MTases-coding genes. Furthermore, one gene that appears to be inactive in the H. pylori UM032 genome during normal growth was characterized by cloning. Consistent with previously-studied H. pylori strains, we show that strain UM032 contains a relatively large number of R-M systems, including some MTase activities with novel specificities. Additional studies are underway to further elucidating the biological significance of the R-M systems in the physiology and pathogenesis of H. pylori.
ISSN:1471-2164
1471-2164
DOI:10.1186/s12864-015-1585-2