{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T21:50:37Z","timestamp":1764193837981},"reference-count":40,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2009,7,1]],"date-time":"2009-07-01T00:00:00Z","timestamp":1246406400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2009,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Infection with wild-type\n            <jats:italic>Listeria monocytogenes<\/jats:italic>\n            activates a host cytosolic surveillance response characterized by the expression of beta interferon (IFN-\u03b2). We performed a genetic screen to identify\n            <jats:italic>L. monocytogenes<\/jats:italic>\n            transposon insertion mutants that induced altered levels of host IFN-\u03b2 expression. One mutant from this screen induced elevated levels of IFN-\u03b2 and harbored a Tn\n            <jats:italic>917<\/jats:italic>\n            insertion upstream of lmo0558. This study identified lmo0558 as the 6-phosphogluconolactonase gene (\n            <jats:italic>pgl<\/jats:italic>\n            ), which encodes the second enzyme in the pentose phosphate pathway.\n            <jats:italic>pgl<\/jats:italic>\n            mutant\n            <jats:italic>L. monocytogenes<\/jats:italic>\n            accumulated and secreted large amounts of gluconate, likely derived from labile 6-phosphogluconolactone, the substrate of Pgl. The\n            <jats:italic>pgl<\/jats:italic>\n            deletion mutant had decreased growth in glucose-limiting minimal medium but grew normally when excess glucose was added. Microarray analysis revealed that the\n            <jats:italic>pgl<\/jats:italic>\n            deletion mutant had increased expression of several \u03b2-glucosidases, consistent with known inhibition of \u03b2-glucosidases by 6-phosphogluconolactone. While growth in macrophages was indistinguishable from that of wild-type bacteria,\n            <jats:italic>pgl<\/jats:italic>\n            mutant\n            <jats:italic>L. monocytogenes<\/jats:italic>\n            exhibited a 15- to 30-fold defect in growth in vivo. In addition,\n            <jats:italic>L. monocytogenes<\/jats:italic>\n            harboring an in-frame deletion of\n            <jats:italic>pgl<\/jats:italic>\n            was more sensitive to oxidative stress. This study identified\n            <jats:italic>L. monocytogenes pgl<\/jats:italic>\n            and provided the first link between the bacterial pentose phosphate pathway and activation of host IFN-\u03b2 expression.\n          <\/jats:p>","DOI":"10.1128\/iai.01511-08","type":"journal-article","created":{"date-parts":[[2009,4,28]],"date-time":"2009-04-28T01:23:00Z","timestamp":1240881780000},"page":"3014-3022","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":15,"title":["<i>Listeria monocytogenes<\/i>\n            6-Phosphogluconolactonase Mutants Induce Increased Activation of a Host Cytosolic Surveillance Pathway"],"prefix":"10.1128","volume":"77","author":[{"given":"Gregory T.","family":"Crimmins","sequence":"first","affiliation":[{"name":"Department of Molecular and Cell Biology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael 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