Role of interspecies transfer of chromosomal genes in the evolution of penicillin resistance in pathogenic and commensal Neisseria species
dc.contributor.author | Bowler, Lucas D. | en_US |
dc.contributor.author | Spratt, Brian G. | en_US |
dc.contributor.author | Smith, John Maynard | en_US |
dc.contributor.author | Zhang, Qian-Yun | en_US |
dc.contributor.author | Zhou, Jiaji | en_US |
dc.date.accessioned | 2006-09-11T19:41:47Z | |
dc.date.available | 2006-09-11T19:41:47Z | |
dc.date.issued | 1992-02 | en_US |
dc.identifier.citation | Spratt, Brian G.; Bowler, Lucas D.; Zhang, Qian-Yun; Zhou, Jiaji; Smith, John Maynard; (1992). "Role of interspecies transfer of chromosomal genes in the evolution of penicillin resistance in pathogenic and commensal Neisseria species." Journal of Molecular Evolution 34(2): 115-125. <http://hdl.handle.net/2027.42/48045> | en_US |
dc.identifier.issn | 0022-2844 | en_US |
dc.identifier.issn | 1432-1432 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/48045 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1556747&dopt=citation | en_US |
dc.description.abstract | The two pathogenic species of Neisseria, N. meningitidis and N. gonorrhoeae , have evolved resistance to penicillin by alterations in chromosomal genes encoding the high molecular weight penicillin-binding proteins, or PBPs. The PBP 2 gene ( penA ) has been sequenced from over 20 Neisseria isolates, including susceptible and resistant strains of the two pathogenic species, and five human commensal species. The genes from penicillin-susceptible strains of N. meningitidis and N. gonorrhoeae are very uniform, whereas those from penicillin-resistant strains consist of a mosaic of regions resembling those in susceptible strains of the same species, interspersed with regions resembling those in one, or in some cases, two of the commensal species. The mosaic structure is interpreted as having arisen from the horizontal transfer, by genetic transformation, of blocks of DNA, usually of a few hundred base pairs. The commensal species identified as donors in these interspecies recombinational events ( N. flavescens and N. cinerea ) are intrinsically more resistant to penicillin than typical isolates of the pathogenic species. Transformation has apparently provided N. meningitidis and N. gonorrhoeae with a mechanism by which they can obtain increased resistance to penicillin by replacing their penA genes (or the relevant parts of them) with the penA genes of related species that fortuitously produce forms of PBP 2 that are less susceptible to inhibition by the antibiotic. The ends of the diverged blocks of DNA in the penA genes of different penicillin-resistant strains are located at the same position more often than would be the case if they represent independent crossovers at random points along the gene. Some of these common crossover points may represent common ancestry, but reasons are given for thinking that some may represent independent events occurring at recombinational hotspots. | en_US |
dc.format.extent | 1167277 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Springer-Verlag | en_US |
dc.subject.other | Mosaic Gene Structure | en_US |
dc.subject.other | Penicillin Resistance | en_US |
dc.subject.other | Microbiology | en_US |
dc.subject.other | Cell Biology | en_US |
dc.subject.other | Life Sciences | en_US |
dc.subject.other | Plant Sciences | en_US |
dc.subject.other | Horizontal Transfer | en_US |
dc.subject.other | Genetic Transformation | en_US |
dc.title | Role of interspecies transfer of chromosomal genes in the evolution of penicillin resistance in pathogenic and commensal Neisseria species | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Natural Resources and Environment | en_US |
dc.subject.hlbsecondlevel | Ecology and Evolutionary Biology | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | School of Biological Sciences, University of Sussex, BN1 9QG, Falmer, Brighton, England; Department of Microbiology and Immunology, University of Michigan Medical School, 48109, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationother | School of Biological Sciences, University of Sussex, BN1 9QG, Falmer, Brighton, England | en_US |
dc.contributor.affiliationother | School of Biological Sciences, University of Sussex, BN1 9QG, Falmer, Brighton, England | en_US |
dc.contributor.affiliationother | School of Biological Sciences, University of Sussex, BN1 9QG, Falmer, Brighton, England | en_US |
dc.contributor.affiliationother | School of Biological Sciences, University of Sussex, BN1 9QG, Falmer, Brighton, England | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 1556747 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/48045/1/239_2004_Article_BF00182388.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF00182388 | en_US |
dc.identifier.source | Journal of Molecular Evolution | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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