{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T18:04:53Z","timestamp":1785434693287,"version":"3.56.0"},"reference-count":69,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2025,6,11]],"date-time":"2025-06-11T00:00:00Z","timestamp":1749600000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,6,11]],"date-time":"2025-06-11T00:00:00Z","timestamp":1749600000000},"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":["1R01 AI027655"],"award-info":[{"award-number":["1R01 AI027655"]}],"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":["1P01 AI063302"],"award-info":[{"award-number":["1P01 AI063302"]}],"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":["R01 GM144694-02"],"award-info":[{"award-number":["R01 GM144694-02"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2025,6,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Listeria monocytogenes (Lm<\/jats:italic>\n                      ) is a Gram-positive, facultative intracellular pathogen that uses both a housekeeping (P1) and stress-activated (Sigma B-dependent) promoter (P2) to express the master virulence regulator PrfA. The Sigma B regulon contains over 300 genes known to respond to different stressors. However, the role of Sigma B in the regulation of\n                      <jats:italic toggle=\"yes\">prfA<\/jats:italic>\n                      during the infection remains uncertain. To define pathways that lead to Sigma B-dependent\n                      <jats:italic toggle=\"yes\">prfA<\/jats:italic>\n                      activation, we performed a genetic screen in L2 fibroblasts using \u0394P1\n                      <jats:italic toggle=\"yes\">Lm<\/jats:italic>\n                      that only has the Sigma B-dependent promoter directly upstream of\n                      <jats:italic toggle=\"yes\">prfA<\/jats:italic>\n                      . The screen identified transposon insertions in a large bacterial sensory organelle known as the stressosome. The absence of functional stressosome components resulted in heterogeneity within bacterial populations, with some bacteria behaving like wild type, while other members of the population exhibited defects in either vacuolar escape and\/or cell-to-cell spread. We show that the heterogeneity of the stressosome mutants cannot be rescued by constitutive activation of PrfA. These data defined the importance of the stressosome in controlling bacterial homogeneity and characterized the function of the stressosome in robust virulence activation during infection. \u0394P1\n                      <jats:italic toggle=\"yes\">Lm<\/jats:italic>\n                      model provides new opportunities to identify host-specific signals necessary for stressosome-dependent signaling during\n                      <jats:italic toggle=\"yes\">Listeria<\/jats:italic>\n                      pathogenesis.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Microbial pathogens must adapt to varying levels of stress to survive. This study uncovered a link between stress sensing and activation of the virulence program in a facultative intracellular pathogen,\n                        <jats:italic toggle=\"yes\">Listeria monocytogenes<\/jats:italic>\n                        . We show that host-imposed stress is sensed by the signaling machinery known as the stressosome to ensure robust and resilient virulence responses\n                        <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                        . Stressosome-dependent activation of the master virulence regulator PrfA was necessary to maintain\n                        <jats:italic toggle=\"yes\">L. monocytogenes<\/jats:italic>\n                        homogeneity within the bacteria population during the transition between early and late stages of intracellular infection. This work also provides a model to further characterize how specific stress stimuli affect bacterial survival within the host\n                        <jats:italic toggle=\"yes\">,<\/jats:italic>\n                        which is critical for our understanding of bacterial pathogenesis.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.00719-25","type":"journal-article","created":{"date-parts":[[2025,4,30]],"date-time":"2025-04-30T21:06:46Z","timestamp":1746047206000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":2,"title":["Stress-dependent activation of the\n                    <i>Listeria monocytogenes<\/i>\n                    virulence program ensures bacterial resilience during infection"],"prefix":"10.1128","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3513-301X","authenticated-orcid":false,"given":"Mariya","family":"Lobanovska","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01an7q238","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular and Cell Biology, University of California, Berkeley","place":["Berkeley, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Feng","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01an7q238","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular and Cell Biology, University of California, Berkeley","place":["Berkeley, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan","family":"Zhang","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01an7q238","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular and Cell Biology, University of California, Berkeley","place":["Berkeley, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allison H.","family":"Williams","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/043mz5j54","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cellular and Molecular Pharmacology, University of California, San Francisco","place":["San Francisco, USA"]},{"id":[{"id":"https:\/\/ror.org\/00knt4f32","id-type":"ROR","asserted-by":"publisher"}],"name":"Chan Zuckerberg Biohub","place":["San Francisco, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1218-2799","authenticated-orcid":true,"given":"Daniel A.","family":"Portnoy","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01an7q238","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular and Cell Biology, University of California, Berkeley","place":["Berkeley, 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