{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T13:49:34Z","timestamp":1791553774317,"version":"4.3.4"},"reference-count":70,"publisher":"American Society for Microbiology","license":[{"start":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T00:00:00Z","timestamp":1791504000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T00:00:00Z","timestamp":1791504000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R35GM124733"],"award-info":[{"award-number":["R35GM124733"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R35GM131762"],"award-info":[{"award-number":["R35GM131762"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["F32AI174818"],"award-info":[{"award-number":["F32AI174818"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01AI177619"],"award-info":[{"award-number":["R01AI177619"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Bacterial gene expression depends on the coordinated regulation of RNA synthesis, processing, and decay. The conserved RNA degradosome scaffold, ribonuclease E (RNase E), assembles into phase-separated bacterial ribonucleoprotein bodies (BR-bodies) through its C-terminal intrinsically disordered region (IDR). This IDR also scaffolds recruitment of degradosome client proteins that carry out post-transcriptional gene regulation. Whether BR-bodies regulate virulence programs to support infection, however, is largely undefined. We show that RNase E of the intracellular pathogen\n                      <jats:italic toggle=\"yes\">Brucella ovis<\/jats:italic>\n                      forms RNA-dependent condensates\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      and phase-separates with RNA\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      , with the IDR necessary and sufficient for BR-body assembly. Deleting the IDR [\n                      <jats:italic toggle=\"yes\">rne<\/jats:italic>\n                      (\u0394IDR)] did not impair growth but sensitized\n                      <jats:italic toggle=\"yes\">Brucella<\/jats:italic>\n                      to host-relevant oxidative and cell-envelope stressors. Transcriptome-wide profiling that simultaneously resolved mRNA decay and processing revealed that BR-bodies primarily accelerate mRNA turnover while stabilizing a distinct subset of transcripts. Notably, BR-bodies control the processing and levels of\n                      <jats:italic toggle=\"yes\">virB<\/jats:italic>\n                      type IV secretion system mRNA and the turnover of its key activators, linking condensate-based RNA regulation to a core virulence pathway. Consistent with\n                      <jats:italic toggle=\"yes\">virB<\/jats:italic>\n                      dysregulation, the\n                      <jats:italic toggle=\"yes\">rne<\/jats:italic>\n                      (\u0394IDR) mutant was severely attenuated in mammalian macrophages. To test whether phase separation is sufficient for BR-body function, we replaced the\n                      <jats:italic toggle=\"yes\">B. ovis<\/jats:italic>\n                      IDR with the highly divergent\n                      <jats:italic toggle=\"yes\">Caulobacter crescentus<\/jats:italic>\n                      IDR. This chimera assembled BR-bodies but rescued fitness incompletely, fully restoring oxidative-stress resistance but not cell-envelope stress resistance or intracellular fitness. BR-bodies therefore link RNA metabolism to\n                      <jats:italic toggle=\"yes\">Brucella<\/jats:italic>\n                      stress resistance and infection, and their full function requires both phase separation and additional native IDR-specific activities, such as degradosome interactions.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Biomolecular condensates are non-membrane-bound organelles that organize biological processes across all domains of life, but their role in bacterial infection is not well characterized. We show that\n                        <jats:italic toggle=\"yes\">Brucella<\/jats:italic>\n                        , an intracellular bacterial pathogen and causative agent of the disease brucellosis, relies on biomolecular condensates called bacterial ribonucleoprotein bodies (BR-bodies) to control RNA stability and regulate gene expression. Without BR-bodies,\n                        <jats:italic toggle=\"yes\">Brucella<\/jats:italic>\n                        is sensitized to host-relevant chemical stresses, cannot properly regulate essential infection machinery, and has severely diminished fitness within mammalian host cells. These results indicate that control of RNA levels by biomolecular condensates is required for\n                        <jats:italic toggle=\"yes\">Brucella<\/jats:italic>\n                        survival within animal hosts, providing evidence that phase separation is a fundamental mechanism underlying\n                        <jats:italic toggle=\"yes\">Brucella<\/jats:italic>\n                        adaptation to the hostile environment encountered during infection.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.01705-26","type":"journal-article","created":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T13:00:15Z","timestamp":1791550815000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["BR-bodies link RNA homeostasis to stress tolerance and intracellular fitness in\n                    <i>Brucella<\/i>"],"prefix":"10.1128","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5201-2279","authenticated-orcid":false,"given":"Kaveendya S.","family":"Mallikaarachchi","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02k40bc56","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biology, Indiana University","place":["Bloomington, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosemary","family":"Northcote","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05hs6h993","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, Genetics, and Immunology, Michigan State University","place":["East Lansing, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Kim","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05hs6h993","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, Genetics, and Immunology, 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