<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ando T</submitter><funding>NIGMS NIH HHS</funding><pagination>295-301</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC141823</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>185(1)</volume><pubmed_abstract>A recently identified Helicobacter pylori gene, hrgA, was previously reported to be present in 70 (33%) of 208 strains examined (T. Ando, T. M. Wassenaar, R. M. Peek, R. A. Aras, A. I. Tschumi, L.-J. Van Doorn, K. Kusugami, and M. J. Blaser, Cancer Res. 62:2385-2389, 2002). Sequence analysis of nine such strains indicated that in each strain hrgA replaced hpyIIIR, which encodes a restriction endonuclease and which, together with the gene for its cognate methyltransferase, constitutes the hpyIII locus. As a consequence of either the hrgA insertion or independent mutations, hpyIIIM function was lost in 11 (5%) of the 208 strains examined, rendering chromosomal DNA sensitive to MboI digestion. The evolutionary history of the locus containing either hpyIII or hrgA was reconstructed. By homolog</pubmed_abstract><journal>Journal of bacteriology</journal><pubmed_title>Evolutionary history of hrgA, which replaces the restriction gene hpyIIIR in the hpyIII locus of Helicobacter pylori.</pubmed_title><pmcid>PMC141823</pmcid><funding_grant_id>R01 GM063270</funding_grant_id><funding_grant_id>R01 GM 63270</funding_grant_id><pubmed_authors>Wassenaar TM</pubmed_authors><pubmed_authors>Ando T</pubmed_authors><pubmed_authors>Blaser MJ</pubmed_authors><pubmed_authors>Aras RA</pubmed_authors><pubmed_authors>Kusugami K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Evolutionary history of hrgA, which replaces the restriction gene hpyIIIR in the hpyIII locus of Helicobacter pylori.</name><description>A recently identified Helicobacter pylori gene, hrgA, was previously reported to be present in 70 (33%) of 208 strains examined (T. Ando, T. M. Wassenaar, R. M. Peek, R. A. Aras, A. I. Tschumi, L.-J. Van Doorn, K. Kusugami, and M. J. Blaser, Cancer Res. 62:2385-2389, 2002). Sequence analysis of nine such strains indicated that in each strain hrgA replaced hpyIIIR, which encodes a restriction endonuclease and which, together with the gene for its cognate methyltransferase, constitutes the hpyIII locus. As a consequence of either the hrgA insertion or independent mutations, hpyIIIM function was lost in 11 (5%) of the 208 strains examined, rendering chromosomal DNA sensitive to MboI digestion. The evolutionary history of the locus containing either hpyIII or hrgA was reconstructed. By homolog</description><dates><release>2003-01-01T00:00:00Z</release><publication>2003 Jan</publication><modification>2025-04-21T14:55:46.026Z</modification><creation>2019-03-26T23:29:36Z</creation></dates><accession>S-EPMC141823</accession><cross_references><pubmed>12486066</pubmed><doi>10.1128/jb.185.1.295-301.2003</doi><doi>10.1128/JB.185.1.295-301.2003</doi></cross_references></HashMap>