{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T01:46:43Z","timestamp":1791942403411,"version":"4.3.4"},"reference-count":86,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2023,12,19]],"date-time":"2023-12-19T00:00:00Z","timestamp":1702944000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2023,12,19]],"date-time":"2023-12-19T00:00:00Z","timestamp":1702944000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"crossref","award":["AI141438"],"award-info":[{"award-number":["AI141438"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000057","name":"HHS | NIH | National Institute of General Medical Sciences","doi-asserted-by":"crossref","award":["GM141242, GM143182"],"award-info":[{"award-number":["GM141242, GM143182"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"crossref"}]},{"name":"GEMS Biology Integration Institute","award":["2022049"],"award-info":[{"award-number":["2022049"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2023,12,19]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Histone-like nucleoid structuring (H-NS) and H-NS-like proteins serve as global gene silencers and work with antagonistic transcriptional activators (counter-silencers) to properly coordinate the expression of virulence genes in pathogenic bacteria. In\n                    <jats:italic>Brucella<\/jats:italic>\n                    , MucR has been proposed as a novel H-NS-like gene silencer, but direct experimental evidence is lacking. Here, we show that MucR serves as an H-NS-like silencer of the\n                    <jats:italic>Brucella abortus<\/jats:italic>\n                    genes encoding the polar autotransporter adhesins BtaE and BmaC, the c-di-GMP-specific phosphodiesterase BpdB, and the quorum-sensing regulator BabR. We also demonstrate that the MarR-type transcriptional activator MdrA can displace MucR from the\n                    <jats:italic>btaE<\/jats:italic>\n                    promoter, supporting the existence of MucR counter-silencers in\n                    <jats:italic>Brucella<\/jats:italic>\n                    . Moreover, our chromatin immunoprecipitation (ChIP)-seq analysis identified 546 MucR enrichment peaks along the genome, including in the promoters of the genes encoding the Type IV secretion machinery and effectors and the quorum-sensing regulator VjbR. Importantly, MucR ChIP-seq peaks overlap with the previously described binding sites for the transcriptional activators VjbR, BvrR, and CtrA suggesting that these regulators serve as MucR counter-silencers and work in concert with MucR to coordinate virulence gene expression in\n                    <jats:italic>Brucella<\/jats:italic>\n                    . In addition, using chromosome conformation capture (Hi-C), we show that like H-NS in\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    , MucR alters the global structure of the\n                    <jats:italic>Brucella<\/jats:italic>\n                    nucleoid. Finally, a copy of the\n                    <jats:italic>E. coli hns<\/jats:italic>\n                    rescues the distinctive growth defect and elevated\n                    <jats:italic>btaE<\/jats:italic>\n                    expression of a\n                    <jats:italic>B. abortus mucR<\/jats:italic>\n                    mutant. Together, these findings solidify the role of MucR as a novel type of H-NS-like protein and suggest that MucR\u2019s gene-silencing properties play a key role in virulence in\n                    <jats:italic>Brucella<\/jats:italic>\n                    .\n                  <\/jats:p>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      Histone-like nucleoid structuring (H-NS) and H-NS-like proteins coordinate host-associated behaviors in many pathogenic bacteria, often through forming silencer\/counter-silencer pairs with signal-responsive transcriptional activators to tightly control gene expression.\n                      <jats:italic>Brucella<\/jats:italic>\n                      and related bacteria do not encode H-NS or homologs of known H-NS-like proteins, and it is unclear if they have other proteins that perform analogous functions during pathogenesis. In this work, we provide compelling evidence for the role of MucR as a novel H-NS-like protein in\n                      <jats:italic>Brucella<\/jats:italic>\n                      . We show that MucR possesses many of the known functions attributed to H-NS and H-NS-like proteins, including the formation of silencer\/counter-silencer pairs to control virulence gene expression and global structuring of the nucleoid. These results uncover a new role for MucR as a nucleoid structuring protein and support the importance of temporal control of gene expression in\n                      <jats:italic>Brucella<\/jats:italic>\n                      and related bacteria.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.02201-23","type":"journal-article","created":{"date-parts":[[2023,10,17]],"date-time":"2023-10-17T12:21:43Z","timestamp":1697545303000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":31,"title":["<i>Brucella<\/i>\n                    MucR acts as an H-NS-like protein to silence virulence genes and structure the nucleoid"],"prefix":"10.1128","volume":"14","author":[{"given":"Ian S.","family":"Barton","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongqing","family":"Ren","sequence":"additional","affiliation":[{"name":"Department of Biology, Indiana University, Bloomington, Indiana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Connor B.","family":"Cribb","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua E.","family":"Pitzer","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ilaria","family":"Baglivo","sequence":"additional","affiliation":[{"name":"Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania \u201cLuigi Vanvitelli\u201d, Caserta, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel W.","family":"Martin","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6458-180X","authenticated-orcid":true,"given":"Xindan","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Biology, Indiana University, Bloomington, Indiana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2101-6928","authenticated-orcid":true,"suffix":"II","given":"R. 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