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Uropathogenic\n            <jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>\n            (UPEC) exhibits such cellular dynamics and has been shown to transition through a series of distinct morphological phenotypes during a urinary tract infection. Here, we report the first systematic spatio-temporal gene expression analysis of the UPEC transition through these phenotypes by using a flow chamber-based\n            <jats:italic>in vitro<\/jats:italic>\n            infection model that simulates conditions in the bladder. This analysis revealed a novel association between the cell division gene\n            <jats:italic>damX<\/jats:italic>\n            and reversible UPEC filamentation. We demonstrate a lack of reversible bacterial filamentation in a\n            <jats:italic>damX<\/jats:italic>\n            deletion mutant\n            <jats:italic>in vitro<\/jats:italic>\n            and absence of a filamentous response by this mutant in a murine model of cystitis. While deletion of\n            <jats:italic>damX<\/jats:italic>\n            abrogated UPEC filamentation and secondary surface colonization in tissue culture and in mouse infections, transient overexpression of\n            <jats:italic>damX<\/jats:italic>\n            resulted in reversible UPEC filamentation. In this study, we identify a hitherto-unknown\n            <jats:italic>damX-<\/jats:italic>\n            mediated mechanism underlying UPEC morphotypical switching. Murine infection studies showed that DamX is essential for establishment of a robust urinary tract infection, thus emphasizing its role as a mediator of virulence. Our study demonstrates the value of an\n            <jats:italic>in vitro<\/jats:italic>\n            methodology, in which uroepithelium infection is closely simulated, when undertaking targeted investigations that are challenging to perform in animal infection models.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            Urinary tract infections (UTIs) are most often caused by uropathogenic\n            <jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>\n            (UPEC) and account for a considerable health care burden. UPEC exhibits a dynamic lifestyle in the course of infection, in which the bacterium transiently adopts alternative morphologies ranging from rod shaped to coccoid and filamentous, rendering it better at immune evasion and host epithelium adhesion. This penchant for morphotype switching might in large measure account for UPEC\u2019s success as a pathogen. In aiming to uncover genes underlying the phenomenon of UPEC morphotype switching, this study identifies\n            <jats:italic>damX<\/jats:italic>\n            , a cell division gene, as a mediator of reversible filamentation during UTI. DamX-mediated filamentation represents an additional pathway for bacterial cell shape control, an alternative to SulA-mediated FtsZ sequestration during\n            <jats:named-content content-type=\"genus-species\">E. coli<\/jats:named-content>\n            uropathogenesis, and hence represents a potential target for combating UTI.\n          <\/jats:p>","DOI":"10.1128\/mbio.00642-16","type":"journal-article","created":{"date-parts":[[2016,8,3]],"date-time":"2016-08-03T01:32:59Z","timestamp":1470187979000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":62,"title":["DamX Controls Reversible Cell Morphology Switching in Uropathogenic Escherichia coli"],"prefix":"10.1128","volume":"7","author":[{"given":"Surabhi","family":"Khandige","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cecilie Antoinette","family":"Asferg","sequence":"additional","affiliation":[{"name":"Research Unit of Clinical Microbiology, Odense University Hospital, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karina Juhl","family":"Rasmussen","sequence":"additional","affiliation":[{"name":"Research Unit of Clinical Microbiology, Odense University Hospital, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin Jakob","family":"Larsen","sequence":"additional","affiliation":[{"name":"Department of Clinical Genetics, Odense University Hospital, Odense, Denmark"},{"name":"Department of Human Genetics, Institute of Clinical Research, University of Southern Denmark, Odense, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Overgaard","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry and 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