{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T15:39:58Z","timestamp":1792510798718,"version":"4.5.0"},"reference-count":66,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T00:00:00Z","timestamp":1791244800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T00:00:00Z","timestamp":1791244800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["2020\/09328-2, 2013\/07467-1, 2024\/14378-0, 2022\/11503-2, 2022\/11051-4, 2021\/12236-5"],"award-info":[{"award-number":["2020\/09328-2, 2013\/07467-1, 2024\/14378-0, 2022\/11503-2, 2022\/11051-4, 2021\/12236-5"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002322","name":"Coordena\u00e7\u00e3o de Aperfei\u00e7oamento de Pessoal de N\u00edvel Superior","doi-asserted-by":"publisher","award":["Finance Code 001,88887.847020\/2023-00"],"award-info":[{"award-number":["Finance Code 001,88887.847020\/2023-00"]}],"id":[{"id":"10.13039\/501100002322","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Spectr"],"published-print":{"date-parts":[[2026,10,6]]},"abstract":"ABSTRACT<\/jats:title>\n \n \n \n The onset of the chronic stage of infection by bacteria in the\n Burkholderia cepacia<\/jats:italic>\n complex depends on the controlled transition to the biofilm-associated lifestyle. In this study, we systematically investigated the effect of all five\n hns<\/jats:italic>\n genes of\n Burkholderia cenocepacia<\/jats:italic>\n H111 on the motile-to-biofilm lifestyle switch and pathogenicity. The\n hns<\/jats:italic>\n genes are distributed across the three replicons (\n hns<\/jats:italic>\n 1.1<\/jats:sub>\n and\n hns<\/jats:italic>\n 1.2<\/jats:sub>\n on chromosome 1,\n hns<\/jats:italic>\n 2<\/jats:sub>\n on chromosome 2, and\n hns<\/jats:italic>\n 3.1<\/jats:sub>\n and\n hns<\/jats:italic>\n 3.2<\/jats:sub>\n on the megaplasmid pC3). We showed that deletion of either\n hns<\/jats:italic>\n 1.1<\/jats:sub>\n or\n hns<\/jats:italic>\n 1.2<\/jats:sub>\n affects cell growth and promotes the cell transition to the biofilm, with the major impact observed in cells lacking\n hns<\/jats:italic>\n 1.2<\/jats:sub>\n . According to a comparative transcriptome analysis, the motile-to-biofilm switch linked to the absence of\n hns<\/jats:italic>\n 1.2<\/jats:sub>\n is supported by downregulation of flagellar and chemotaxis genes and upregulation of several genes involved in biofilm formation. In contrast, biofilm-related genes were downregulated; biofilm formation was reduced; and motility was increased in cells lacking\n hns<\/jats:italic>\n 3.1<\/jats:sub>\n . An opposite impact of\n hns<\/jats:italic>\n 1.2<\/jats:sub>\n and\n hns<\/jats:italic>\n 3.1<\/jats:sub>\n on the motile-to-biofilm transition was also supported by using cells expressing these\n hns<\/jats:italic>\n genes at high levels. Furthermore,\n hns<\/jats:italic>\n 3.1<\/jats:sub>\n and\n hns<\/jats:italic>\n 1.1<\/jats:sub>\n were shown to play a role in bacterial virulence in the\n Galleria mellonella<\/jats:italic>\n infection model. Therefore, this study uncovers\n hns<\/jats:italic>\n genes as new players of the motile-to-biofilm transition in\n B. cenocepacia<\/jats:italic>\n .\n <\/jats:p>\n <\/jats:sec>\n \n IMPORTANCE<\/jats:title>\n \n Several opportunistic pathogenic bacteria can thrive as motile, free-living cells in soil and water, as well as in biofilm in their hosts. This includes the closely related species comprising the\n Burkholderia cepacia<\/jats:italic>\n complex, which chronically colonize the airway in individuals with cystic fibrosis. Over the last two decades, the number of genes involved in the control of the motile-to-biofilm lifestyle switch has increased in this bacterial group, particularly in\n Burkholderia cenocepacia<\/jats:italic>\n . In the present study, we uncover three\n hns<\/jats:italic>\n genes that participate in the motile-to-biofilm lifestyle switch in\n B. cenocepacia<\/jats:italic>\n H111 under the conditions tested. While two chromosomally encoded\n hns<\/jats:italic>\n genes work to maintain cells at the motile stage, a megaplasmid-encoded\n hns<\/jats:italic>\n gene facilitates the cell transition to biofilm. By systematically investigating all five\n hns<\/jats:italic>\n genes, we considerably expand our understanding of the control of the motile-to-biofilm lifestyle switch in the\n Burkholderia cepacia<\/jats:italic>\n complex.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1128\/spectrum.00344-26","type":"journal-article","created":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T16:43:31Z","timestamp":1788367411000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["A functional interplay of\n hns<\/i>\n genes governs the control of the motile-to-biofilm lifestyle switch in\n Burkholderia cenocepacia<\/i>"],"prefix":"10.1128","volume":"14","author":[{"given":"Ana J\u00falia Virg\u00edlio","family":"Tonhetta","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04wffgt70","id-type":"ROR","asserted-by":"publisher"}],"name":"Departamento de Gen\u00e9tica, Evolu\u00e7\u00e3o, Microbiologia e Imunologia, 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