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The importance of PknF for the virulence of Mtb\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      is not known. Here, we demonstrate that the Mtb CDC1551 deletion mutant of\n                      <jats:italic toggle=\"yes\">pknF<\/jats:italic>\n                      (\u2206\n                      <jats:italic toggle=\"yes\">pknF<\/jats:italic>\n                      ) expresses significantly increased levels of the lipid pthiocerol dimycoserosate (PDIM), a polyketide lipid with pro-virulence properties. The \u2206\n                      <jats:italic toggle=\"yes\">pknF<\/jats:italic>\n                      mutant strain compared with the Mtb and complemented strains showed a 100-fold increase in growth at day 28 and about a 10-fold increase in growth at days 90\u201398 in the lungs of mice. The increase in pulmonary bacterial loads after infection with the \u2206\n                      <jats:italic toggle=\"yes\">pknF<\/jats:italic>\n                      strain was conserved even in\n                      <jats:italic toggle=\"yes\">Nlrp3<\/jats:italic>\n                      -deficient mice, arguing that PknF modulates Mtb virulence independently of NLRP3-inflammasome activation in mice. Staining of lung sections revealed increased inflammation in the lungs of \u2206\n                      <jats:italic toggle=\"yes\">pknF<\/jats:italic>\n                      strain-infected mice when compared with Mtb and the complemented mutant strain. Highly susceptible B6.Sst1\n                      <jats:sup>S<\/jats:sup>\n                      mice displayed decreased host resistance, with significantly decreased survival when infected with the \u2206\n                      <jats:italic toggle=\"yes\">pknF<\/jats:italic>\n                      strain compared to the complemented strain or Mtb. In conclusion, our data suggest that expression of PknF, as a modulator of multiple downstream effector proteins, restricts the virulence of Mtb in the lungs of mice through an NLRP3 inflammasome-independent mechanism, but potentially via suppressing production of the virulence lipid, PDIM.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/iai.00698-25","type":"journal-article","created":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T13:00:19Z","timestamp":1785157219000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Protein kinase F regulates the virulence of\n                    <i>Mycobacterium tuberculosis<\/i>"],"prefix":"10.1128","volume":"94","author":[{"given":"Flor","family":"Torres-Juarez","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/043z4tv69","id-type":"ROR","asserted-by":"publisher"}],"name":"Inflammation and Innate Immunity Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases","place":["Bethesda, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0046-0045","authenticated-orcid":true,"given":"Shivangi","family":"Rastogi","sequence":"additional","affiliation":[{"name":"Department of Cell Biology and Molecular Genetics, University of Maryland","place":["College Park, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Young","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Immunity and Inflammation, Brigham and Women\u2019s Hospital, Harvard Medical School","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashton T.","family":"Belew","sequence":"additional","affiliation":[{"name":"Department of Cell Biology and Molecular Genetics, University of Maryland","place":["College Park, USA"]},{"name":"Center for Bioinformatics and Computational Biology, University of Maryland Institute for Advanced Computer Studies, University of Maryland","place":["College Park, USA"]},{"name":"Center for Bioinformatics, University of Maryland Institute for Health Computing","place":["North Bethesda, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul J.","family":"Baker","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/043z4tv69","id-type":"ROR","asserted-by":"publisher"}],"name":"Inflammation and Innate Immunity Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases","place":["Bethesda, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Viplov K.","family":"Biswas","sequence":"additional","affiliation":[{"name":"Department of Cell Biology and Molecular Genetics, University of Maryland","place":["College Park, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shannon E.","family":"Khan","sequence":"additional","affiliation":[{"name":"Department of Cell Biology and Molecular Genetics, University of Maryland","place":["College Park, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7970-3312","authenticated-orcid":true,"given":"Najib M.","family":"El-Sayed","sequence":"additional","affiliation":[{"name":"Department of Cell Biology and Molecular Genetics, University of Maryland","place":["College Park, USA"]},{"name":"Center for Bioinformatics and Computational Biology, University of Maryland Institute for Advanced Computer Studies, University of Maryland","place":["College Park, USA"]},{"name":"Center for Bioinformatics, University of Maryland Institute for Health Computing","place":["North Bethesda, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D. 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