Show simple item record

dc.contributor.authorEijkelkamp, Bart A
dc.contributor.authorStroeher, Uwe Horst
dc.contributor.authorHassan, Karl Adam
dc.contributor.authorElbourne, Liam DH
dc.contributor.authorPaulsen, Ian T
dc.contributor.authorBrown, Melissa Hackett
dc.date.accessioned2013-08-08T01:56:33Z
dc.date.available2013-08-08T01:56:33Z
dc.date.issued2013-05-06
dc.identifier.citationEijkelkamp, B.A., Stroeher, U.H., Hassan, K.A., Elbourne, L.D.H., Paulsen, I.T. and Brown, M.H., 2013. H-NS plays a role in expression of Acinetobacter baumannii virulence features. Infection and Immunity, 81(7), 2574-2583.en
dc.identifier.issn0019-9567
dc.identifier.urihttp://hdl.handle.net/2328/26916
dc.description.abstractAcinetobacter baumannii has become a major problem in the clinical setting with the prevalence of infections caused by multidrug-resistant strains on the increase. Nevertheless, only a limited number of molecular mechanisms involved in the success of A. baumannii as a human pathogen have been described. In this study, we examined the virulence features of a hypermotile derivative of A. baumannii strain ATCC 17978, which was found to display enhanced adherence to human pneumocytes and elevated levels of lethality toward Caenorhabditis elegans nematodes. Analysis of cellular lipids revealed modifications to the fatty acid composition, providing a possible explanation for the observed changes in hydrophobicity and subsequent alteration in adherence and motility. Comparison of the genome sequences of the hypermotile variant and parental strain revealed that an insertion sequence had disrupted an hns-like gene in the variant. This gene encodes a homologue of the histone-like nucleoid structuring (H-NS) protein, a known global transcriptional repressor. Transcriptome analysis identified the global effects of this mutation on gene expression, with major changes seen in the autotransporter Ata, a type VI secretion system, and a type I pilus cluster. Interestingly, isolation and analysis of a second independent hypermotile ATCC 17978 variant revealed a mutation to a residue within the DNA binding region of H-NS. Taken together, these mutants indicate that the phenotypic and transcriptomic differences seen are due to loss of regulatory control effected by H-NS.en
dc.description.sponsorshipThis work was supported by project grant 535053 to M.H.B. and I.T.P. from the National Health and Medical Research Council, Australia. B.A.E. is the recipient of a School of Biological Sciences Endeavor International Postgraduate Research Scholarship, and K.A.H. is supported by an APD fellowship from the Australian Research Council (DP110102680).en
dc.language.isoen
dc.publisherAmerican Society for Microbiologyen
dc.relationhttp://purl.org/au-research/grants/nhmrc/535053en
dc.rightsASM grants the author the right to post his/her article (after publication by ASM) on the author’s personal or university-hosted website, but not on any corporate, government, or similar website, without ASM’s prior permission, provided that proper credit is given to the original ASM publication.en
dc.subjectMicrobiologyen
dc.subjectInfectionen
dc.subjectDrug resistanceen
dc.titleH-NS plays a role in expression of Acinetobacter baumannii virulence featuresen
dc.typeArticleen
dc.relation.grantnumberNHMRC/535053en
dc.identifier.doihttps://doi.org/10.1128/IAI.00065-13en
dc.rights.holderCopyright © 2013, American Society for Microbiology. All Rights Reserveden
dc.rights.licenseIn Copyright
local.contributor.authorOrcidLookupBrown, Melissa Hackett: https://orcid.org/0000-0001-6461-7550en_US


Files in this item

Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail

This item appears in the following Collection(s)

Show simple item record