{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T07:56:38Z","timestamp":1787730998076,"version":"build-2784847793"},"reference-count":47,"publisher":"American Society for Microbiology","issue":"11","license":[{"start":{"date-parts":[[2017,6,1]],"date-time":"2017-06-01T00:00:00Z","timestamp":1496275200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["HE2854\/5-2"],"award-info":[{"award-number":["HE2854\/5-2"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Bacteriol"],"published-print":{"date-parts":[[2017,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Legionella oakridgensis<\/jats:named-content>\n            causes Legionnaires' disease but is known to be less virulent than\n            <jats:named-content content-type=\"genus-species\">Legionella pneumophila<\/jats:named-content>\n            .\n            <jats:named-content content-type=\"genus-species\">L. oakridgensis<\/jats:named-content>\n            is one of the\n            <jats:named-content content-type=\"genus-species\">Legionella<\/jats:named-content>\n            species that is nonflagellated. The genes of the flagellar regulon are absent, except those encoding the alternative sigma-28 factor (FliA) and its anti-sigma-28 factor (FlgM). Similar to\n            <jats:named-content content-type=\"genus-species\">L. oakridgensis<\/jats:named-content>\n            ,\n            <jats:named-content content-type=\"genus-species\">Legionella adelaidensis<\/jats:named-content>\n            and\n            <jats:named-content content-type=\"genus-species\">Legionella londiniensis<\/jats:named-content>\n            , located in the same phylogenetic clade, have no flagellar regulon, although both are positive for\n            <jats:italic>fliA<\/jats:italic>\n            and\n            <jats:italic>flgM<\/jats:italic>\n            . Here, we investigated the role and function of both genes to better understand the role of FliA, the positive regulator of flagellin expression, in nonflagellated strains. We demonstrated that the FliA gene of\n            <jats:named-content content-type=\"genus-species\">L. oakridgensis<\/jats:named-content>\n            encodes a functional sigma-28 factor that enables the transcription start from the sigma-28-dependent promoter site. The investigations have shown that FliA is necessary for full fitness of\n            <jats:named-content content-type=\"genus-species\">L. oakridgensis<\/jats:named-content>\n            . Interestingly, expression of FliA-dependent genes depends on the growth phase and temperature, as already shown for\n            <jats:named-content content-type=\"genus-species\">L. pneumophila<\/jats:named-content>\n            strains that are flagellated. In addition, we demonstrated that FlgM is a negative regulator of FliA-dependent gene expression. FlgM seems to be degraded in a growth-phase- and temperature-dependent manner, instead of being exported into the medium as reported for most bacteria. The degradation of FlgM leads to an increase of FliA activity.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            A less virulent\n            <jats:named-content content-type=\"genus-species\">Legionella<\/jats:named-content>\n            species,\n            <jats:named-content content-type=\"genus-species\">L. oakridgensis<\/jats:named-content>\n            , causes Legionnaires' disease and is known to not have flagella, even though\n            <jats:named-content content-type=\"genus-species\">L. oakridgensis<\/jats:named-content>\n            has the regulator of flagellin expression (FliA). This protein has been shown to be involved in the expression of virulence factors. Thus, the strain was chosen for use in this investigation to search for FliA target genes and to identify putative virulence factors of\n            <jats:named-content content-type=\"genus-species\">L. oakridgensis<\/jats:named-content>\n            . One of the five major target genes of FliA identified here encodes the anti-FliA sigma factor FlgM. Interestingly, in contrast to most homologs in other bacteria, FlgM in\n            <jats:named-content content-type=\"genus-species\">L. oakridgensis<\/jats:named-content>\n            seems not to be transported from the cell so that FliA gets activated. In\n            <jats:named-content content-type=\"genus-species\">L. oakridgensis<\/jats:named-content>\n            , FlgM seems to be degraded by protease activities.\n          <\/jats:p>","DOI":"10.1128\/jb.00018-17","type":"journal-article","created":{"date-parts":[[2017,3,21]],"date-time":"2017-03-21T00:25:39Z","timestamp":1490055939000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":6,"title":["Functional Analysis of the Alternative Sigma-28 Factor FliA and Its Anti-Sigma Factor FlgM of the Nonflagellated Legionella Species L. oakridgensis"],"prefix":"10.1128","volume":"199","author":[{"given":"Hana","family":"Tlap\u00e1k","sequence":"first","affiliation":[{"name":"Cellular Interactions of Bacterial Pathogens, ZBS 2, Robert Koch Institute, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kerstin","family":"Rydzewski","sequence":"additional","affiliation":[{"name":"Cellular Interactions of Bacterial Pathogens, ZBS 2, Robert Koch Institute, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tino","family":"Schulz","sequence":"additional","affiliation":[{"name":"University Tissue Bank, Institute of Transfusion Medicine, Charit\u00e9-Universit\u00e4tsmedizin, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dennis","family":"Weschka","sequence":"additional","affiliation":[{"name":"Cellular Interactions of Bacterial Pathogens, ZBS 2, Robert Koch Institute, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva","family":"Schunder","sequence":"additional","affiliation":[{"name":"University Tissue Bank, Institute of Transfusion Medicine, Charit\u00e9-Universit\u00e4tsmedizin, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klaus","family":"Heuner","sequence":"additional","affiliation":[{"name":"Cellular Interactions of Bacterial Pathogens, ZBS 2, Robert Koch Institute, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.53.3.553-559.1986"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/aem.45.2.536-545.1983"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.38.8.3128-3130.2000"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijmm.2013.07.003"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/aem.51.2.422-424.1986"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/aem.63.4.1219-1224.1997"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1139\/w11-126"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.63.7.2499-2507.1995"},{"key":"e_1_3_3_10_2","first-page":"101","volume-title":"Legionella- molecular microbiology","author":"Heuner K","year":"2008","unstructured":"Heuner K Albert-Weissenberger C . 2008. 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