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In bacteria, one mechanism of post-transcriptional regulation involves the binding of small, non-coding RNAs (sRNAs) to target mRNAs to regulate their translation into protein. This regulation generally includes an RNA-binding protein that facilitates the sRNA::mRNA interaction. In the etiological agent of Lyme disease,\n                      <jats:italic toggle=\"yes\">Borreliella burgdorferi<\/jats:italic>\n                      , over 400 temperature-dependent sRNAs have been identified. Here, we characterized the sRNA SR0735, which is upregulated at 37\u00b0C (characteristic of mammalian infection). Transcriptomic and proteomic analyses revealed that deleting SR0735 in\n                      <jats:italic toggle=\"yes\">B. burgdorferi<\/jats:italic>\n                      resulted in reduced production of virulence-associated, RpoS-dependent proteins due to a reduction of RpoS and its upstream regulator BosR. We thus renamed SR0735 as BasA for\n                      <jats:underline>B<\/jats:underline>\n                      osR-\n                      <jats:underline>a<\/jats:underline>\n                      ssociated\n                      <jats:underline>s<\/jats:underline>\n                      RNA locus\n                      <jats:underline>A<\/jats:underline>\n                      . Consistent with previous studies that identified BosR as an RNA-binding protein, we demonstrate here that BosR can bind BasA\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      . Importantly, the loss of BasA significantly attenuated\n                      <jats:italic toggle=\"yes\">B. burgdorferi<\/jats:italic>\n                      infectivity during murine infection, which is consistent with the reduced levels of BosR and RpoS observed. The emerging model suggests that BasA is required for optimal levels of BosR protein through the post-transcriptional regulation of\n                      <jats:italic toggle=\"yes\">bosR<\/jats:italic>\n                      mRNA, which, in turn, promotes the production of RpoS and its downstream genes required for mammalian infectivity and pathogenesis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/iai.00026-26","type":"journal-article","created":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T13:45:41Z","timestamp":1773150341000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":3,"title":["The\n                    <i>Borreliella burgdorferi<\/i>\n                    BosR-associated small non-coding RNA BasA regulates virulence"],"prefix":"10.1128","volume":"94","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-0306-2481","authenticated-orcid":false,"given":"Brittany 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