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Despite this, little is known about the biology, host-pathogen interactions, or outcomes of these infections, and this has led to uncertain guidelines for clinical management of\n                      <jats:italic toggle=\"yes\">Candida<\/jats:italic>\n                      CAUTIs. Here, we develop the first physiologically relevant artificial urine medium (AUM) that supports fungal growth in a manner similar to, but more consistent than, human urine samples. We demonstrate that human catheter-associated (CA) clinical isolates of\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      exhibit environment-dependent fluconazole resistance: many isolates determined to be susceptible by standard CLSI testing in RPMI (MIC \u2264 2 \u00b5g\/mL) were fully resistant (MIC \u2265 128 \u00b5g\/mL) when grown in pooled human urine or AUM, complicating clinical management, which is based on catheter exchange and fluconazole treatment. Transcriptomic profiling of biofilms formed in AUM revealed a remarkably convergent upregulation of efflux and detoxification processes across clinical isolates with diverse biofilm phenotypes. Whole-genome sequencing of the CA isolates identified variant alleles of transcriptional regulators of drug efflux, including\n                      <jats:italic toggle=\"yes\">MRR1<\/jats:italic>\n                      , that have been previously associated with antifungal resistance. A competition assay confirmed that Mrr1 provides a fitness advantage in urine and AUM in a urea-dependent manner. Thus, we show that the urinary environment promotes a unique biofilm differentiation program and selects for adaptations that increase drug resistance and would be predicted to render standard treatment regimens ineffective.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Catheter-associated urinary tract infections are the most common nosocomial infection in the United States, and\n                        <jats:italic toggle=\"yes\">Candida albicans<\/jats:italic>\n                        is one of the most frequently isolated organisms from these infections. Despite this high prevalence, few molecular studies have examined\n                        <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                        biology in the urinary environment, and recommendations for clinical management lack robust evidence. Here, we show that clinical catheter-associated isolates of\n                        <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                        identified as susceptible to fluconazole by standard clinical microbiology testing were resistant when grown in human or artificial urine. We identified transcriptional responses intrinsic to the urinary environment that produce this environment-specific resistance phenotype. Biofilm growth in the urinary environment induces cellular processes for efflux and detoxification. These findings suggest that standard susceptibility testing may not predict fluconazole efficacy in the urinary tract and underscore the need for niche-informed approaches to antifungal management of these common infections.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.01785-26","type":"journal-article","created":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T13:01:06Z","timestamp":1789390866000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["The catheterized urinary tract selects for\n                    <i>MRR1<\/i>\n                    -mediated efflux and fluconazole resistance in\n                    <i>Candida albicans<\/i>\n                    biofilms"],"prefix":"10.1128","volume":"17","author":[{"given":"Shane A.","family":"Cristy","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03gds6c39","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Molecular Genetics, The University of Texas Health Science Center at Houston","place":["Houston, USA"]},{"name":"Microbiology and Infectious Diseases Program, MD Anderson UTHealth Graduate School of Biomedical Sciences","place":["Houston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0079-3261","authenticated-orcid":true,"given":"Jennifer N.","family":"Walker","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03gds6c39","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Molecular Genetics, The University of Texas Health Science Center at Houston","place":["Houston, USA"]},{"name":"Microbiology and Infectious Diseases Program, MD Anderson UTHealth Graduate School of Biomedical Sciences","place":["Houston, USA"]},{"id":[{"id":"https:\/\/ror.org\/03gds6c39","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Epidemiology, School of Public Health, University of Texas Health Science Center at Houston","place":["Houston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7881-8027","authenticated-orcid":true,"given":"Michael C.","family":"Lorenz","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03gds6c39","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Molecular Genetics, The University of Texas Health Science Center at Houston","place":["Houston, USA"]},{"name":"Microbiology and Infectious Diseases Program, MD Anderson UTHealth Graduate School of Biomedical Sciences","place":["Houston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_6_2_2","doi-asserted-by":"publisher","DOI":"10.3201\/eid0702.010240"},{"key":"e_1_3_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/s0002-9343(00)00531-3"},{"key":"e_1_3_6_4_2","unstructured":"CDC. 2025. 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