{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T00:53:18Z","timestamp":1785372798796,"version":"3.55.0"},"reference-count":39,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2017,5,1]],"date-time":"2017-05-01T00:00:00Z","timestamp":1493596800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2017,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:named-content content-type=\"genus-species\">Neisseria meningitidis<\/jats:named-content>is a commensal microbe that colonizes the human nasopharynx but occasionally invades the bloodstream to cause life-threatening infection.<jats:named-content content-type=\"genus-species\">N. meningitidis<\/jats:named-content>MC58<jats:italic>NMB0419<\/jats:italic>encodes a Sel1-like repeat (SLR)-containing protein, previously implicated in invasion of epithelial cells. A gene-regulatory function was revealed in<jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>expressing plasmid-borne<jats:italic>NMB0419<\/jats:italic>and showing significantly increased epithelial adherence compared to the wild type, due to increased expression of mannose-sensitive type 1 pili. While a meningococcal<jats:italic>NMB0419<\/jats:italic>mutant did not have altered epithelial adherence, in a transcriptome-wide comparison of the wild type and an<jats:italic>NMB0419<\/jats:italic>mutant, a large proportion of genes differentially regulated in the mutant were involved in iron acquisition and metabolism. Fifty-one percent and 38% of genes, respectively, up- and downregulated in the<jats:italic>NMB0419<\/jats:italic>mutant had previously been identified as being induced and repressed by meningococcal Fur. An<jats:italic>in vitro<\/jats:italic>growth defect of the<jats:italic>NMB0419<\/jats:italic>mutant under iron restriction was consistent with the downregulation of<jats:italic>tbpAB<\/jats:italic>and<jats:italic>hmbR<\/jats:italic>, while an intraepithelial replication defect was consistent with the downregulation of<jats:italic>tonB<\/jats:italic>,<jats:italic>exbB<\/jats:italic>, and<jats:italic>exbD<\/jats:italic>, based on a known phenotype of a meningococcal<jats:italic>tonB<\/jats:italic>mutant. Disruption of the N-terminal NMB0419 signal peptide, predicted to export the protein beyond the cytoplasmic membrane, resulted in loss of functional traits in<jats:named-content content-type=\"genus-species\">N. meningitidis<\/jats:named-content>and<jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>. Our study indicates that the expression of<jats:italic>NMB0419<\/jats:italic>is associated with transcriptional changes counterbalancing the regulatory function of Fur, offering a new perspective on regulatory mechanisms involved in meningococcal interaction with epithelial cells, and suggests new insights into the roles of SLR-containing genes in other bacteria.<\/jats:p>","DOI":"10.1128\/iai.00574-16","type":"journal-article","created":{"date-parts":[[2017,3,7]],"date-time":"2017-03-07T01:40:52Z","timestamp":1488850852000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":6,"title":["Inactivation of<i>NMB0419<\/i>, Encoding a Sel1-Like Repeat (SLR) Protein, in Neisseria meningitidis Is Associated with Differential Expression of Genes Belonging to the Fur Regulon and Reduced Intraepithelial Replication"],"prefix":"10.1128","volume":"85","author":[{"given":"Ming-Shi","family":"Li","sequence":"first","affiliation":[{"name":"Section of Paediatrics, Department of Medicine, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6368-4724","authenticated-orcid":false,"given":"Paul R.","family":"Langford","sequence":"additional","affiliation":[{"name":"Section of Paediatrics, Department of Medicine, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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