{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T22:03:29Z","timestamp":1791842609668,"version":"4.3.4"},"update-to":[{"DOI":"10.1371\/journal.ppat.1012492","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2025,5,5]],"date-time":"2025-05-05T00:00:00Z","timestamp":1746403200000}}],"reference-count":85,"publisher":"Public Library of Science (PLoS)","issue":"4","license":[{"start":{"date-parts":[[2025,4,15]],"date-time":"2025-04-15T00:00:00Z","timestamp":1744675200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["T32GM140935"],"award-info":[{"award-number":["T32GM140935"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["T32GM008692"],"award-info":[{"award-number":["T32GM008692"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100015691","name":"Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["T32AI055397"],"award-info":[{"award-number":["T32AI055397"]}],"id":[{"id":"10.13039\/100015691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100015691","name":"Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01AI184369"],"award-info":[{"award-number":["R01AI184369"]}],"id":[{"id":"10.13039\/100015691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100015691","name":"Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R21AI173738"],"award-info":[{"award-number":["R21AI173738"]}],"id":[{"id":"10.13039\/100015691","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100015691","name":"Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01AI137070"],"award-info":[{"award-number":["R01AI137070"]}],"id":[{"id":"10.13039\/100015691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p>\n                    The metabolism of bacterial pathogens is exquisitely evolved to support virulence in the nutrient-limiting host. Many bacterial pathogens utilize bipartite metabolism to support intracellular growth by splitting carbon utilization between two carbon sources and dividing flux to distinct metabolic needs. For example, previous studies suggest that the professional cytosolic pathogen\n                    <jats:italic>Listeria monocytogenes<\/jats:italic>\n                    (\n                    <jats:italic>L. monocytogenes<\/jats:italic>\n                    ) utilizes glycerol and hexose phosphates (e.g., Glucose-6-Phosphate) as catabolic and anabolic carbon sources in the host cytosol, respectively. However, the role of this putative bipartite metabolism in\n                    <jats:italic>L. monocytogenes<\/jats:italic>\n                    virulence has not been fully assessed. Here, we demonstrate that when\n                    <jats:italic>L. monocytogenes<\/jats:italic>\n                    is unable to consume either glycerol (\u0394\n                    <jats:italic>glpD<\/jats:italic>\n                    \/\u0394\n                    <jats:italic>golD<\/jats:italic>\n                    ), hexose phosphates (\u0394\n                    <jats:italic>uhpT<\/jats:italic>\n                    ), or both (\u0394\n                    <jats:italic>glpD<\/jats:italic>\n                    \/\u0394\n                    <jats:italic>golD<\/jats:italic>\n                    \/\u0394\n                    <jats:italic>uhpT<\/jats:italic>\n                    ), it is still able to grow in the host cytosol and is 10- to 100-fold attenuated\n                    <jats:italic>in vivo<\/jats:italic>\n                    suggesting that\n                    <jats:italic>L. monocytogenes<\/jats:italic>\n                    consumes alternative carbon source(s) in the host. An\n                    <jats:italic>in vitro<\/jats:italic>\n                    metabolic screen using BioLog\u2019s phenotypic microarrays unexpectedly demonstrated that WT and PrfA* (G145S)\n                    <jats:italic>L. monocytogenes<\/jats:italic>\n                    , a strain with constitutive virulence gene expression, use phosphotransferase system (PTS) mediated carbon sources. These findings contrast with the existing metabolic model that cytosolic\n                    <jats:italic>L. monocytogenes<\/jats:italic>\n                    expressing PrfA does not use PTS mediated carbon sources. We next demonstrate that two independent and universal phosphocarrier proteins (PtsI [EI] and PtsH [HPr]), essential for the function of all PTS, are critical for intracellular growth and virulence\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Constitutive virulence gene expression using a PrfA* (G145S) allele in \u0394\n                    <jats:italic>glpD<\/jats:italic>\n                    \/\u0394\n                    <jats:italic>golD<\/jats:italic>\n                    \/\u0394\n                    <jats:italic>uhpT<\/jats:italic>\n                    and \u0394\n                    <jats:italic>ptsI<\/jats:italic>\n                    failed to rescue\n                    <jats:italic>in vivo<\/jats:italic>\n                    virulence defects suggesting phenotypes are due to metabolic disruption and not virulence gene regulation. Finally,\n                    <jats:italic>in vivo<\/jats:italic>\n                    attenuation of \u0394\n                    <jats:italic>ptsI and<\/jats:italic>\n                    \u0394\n                    <jats:italic>ptsH<\/jats:italic>\n                    was additive to \u0394\n                    <jats:italic>glpD<\/jats:italic>\n                    \/\u0394\n                    <jats:italic>golD<\/jats:italic>\n                    \/\u0394\n                    <jats:italic>uhpT<\/jats:italic>\n                    , suggesting that hexose phosphates and glycerol and PTS mediated carbon source are relevant metabolites. Taken together, these studies indicate that PTS are critical virulence factors for the cytosolic growth and virulence of\n                    <jats:italic>L. monocytogenes<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1371\/journal.ppat.1012492","type":"journal-article","created":{"date-parts":[[2025,4,15]],"date-time":"2025-04-15T13:41:16Z","timestamp":1744724476000},"page":"e1012492","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":18,"title":["Listeria monocytogenes requires phosphotransferase systems to facilitate intracellular growth and virulence"],"prefix":"10.1371","volume":"21","author":[{"given":"Matthew J.","family":"Freeman","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noah J.","family":"Eral","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9367-794X","authenticated-orcid":true,"given":"John-Demian","family":"Sauer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"340","published-online":{"date-parts":[[2025,4,15]]},"reference":[{"issue":"21","key":"ppat.1012492.ref001","doi-asserted-by":"crossref","first-page":"12221","DOI":"10.1073\/pnas.211106398","article-title":"Microinjection and growth of bacteria in the cytosol of mammalian host cells","volume":"98","author":"M Goetz","year":"2001","journal-title":"Proc Natl Acad Sci USA"},{"issue":"9","key":"ppat.1012492.ref002","doi-asserted-by":"crossref","first-page":"3481","DOI":"10.1073\/pnas.1121286109","article-title":"The protein SdhA maintains the integrity of the Legionella -containing vacuole","volume":"109","author":"EA 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