{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T02:32:09Z","timestamp":1791340329735,"version":"4.3.1"},"reference-count":42,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2015,7,4]],"date-time":"2015-07-04T00:00:00Z","timestamp":1435968000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"NIH","award":["AI44198"],"award-info":[{"award-number":["AI44198"]}]},{"DOI":"10.13039\/100009429","name":"NRSA","doi-asserted-by":"crossref","award":["F32-AI108097"],"award-info":[{"award-number":["F32-AI108097"]}],"id":[{"id":"10.13039\/100009429","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Microbiology"],"published-print":{"date-parts":[[2015,9]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Bacteria encode heat shock proteins that aid in survival during stressful growth conditions. In addition, the major heat shock proteins of the intracellular bacterium <jats:styled-content style=\"fixed-case\"><jats:italic>C<\/jats:italic><\/jats:styled-content><jats:italic>hlamydia trachomatis<\/jats:italic> have been associated with immune pathology and disease. We developed a <jats:styled-content style=\"fixed-case\">ChIP<\/jats:styled-content>\u2010q<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> method to study the regulation of chlamydial heat shock gene regulation during an intracellular infection. This approach allowed us to show that chlamydial heat shock genes are regulated by the transcription factor <jats:styled-content style=\"fixed-case\">HrcA<\/jats:styled-content> within an infected cell, providing validation for previous <jats:italic>in vitro<\/jats:italic> findings. Induction of chlamydial heat shock gene expression by elevated temperature was due to loss of <jats:styled-content style=\"fixed-case\">HrcA<\/jats:styled-content> binding to heat shock promoters, supporting a mechanism of derepression. This heat shock response was rapid, whereas recovery of <jats:styled-content style=\"fixed-case\">HrcA<\/jats:styled-content> binding and return to non\u2010stress transcript levels occurred more slowly. We also found that control of heat shock gene expression was differentially regulated over the course of the intracellular <jats:styled-content style=\"fixed-case\"><jats:italic>C<\/jats:italic><\/jats:styled-content><jats:italic>hlamydia<\/jats:italic> infection. There was evidence of <jats:styled-content style=\"fixed-case\">HrcA<\/jats:styled-content>\u2010mediated regulation of heat shock genes throughout the chlamydial developmental cycle, but the level of repression was lower at early times. This is the first study of <jats:styled-content style=\"fixed-case\"><jats:italic>C<\/jats:italic><\/jats:styled-content><jats:italic>hlamydia<\/jats:italic>\u2010infected cells showing the effect of an environmental signal on transcription factor\u2010<jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> binding and target gene expression in the bacterium.<\/jats:p>","DOI":"10.1111\/mmi.13093","type":"journal-article","created":{"date-parts":[[2015,6,15]],"date-time":"2015-06-15T10:49:21Z","timestamp":1434365361000},"page":"1158-1167","source":"Crossref","is-referenced-by-count":26,"title":["Transcriptional regulation of the <scp><i>C<\/i><\/scp><i>hlamydia<\/i> heat shock stress response in an intracellular infection"],"prefix":"10.1111","volume":"97","author":[{"given":"Brett R.","family":"Hanson","sequence":"first","affiliation":[{"name":"Department of Microbiology and Molecular Genetics University of California  Irvine CA 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