{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T13:10:58Z","timestamp":1788959458412,"version":"build-2803163510"},"reference-count":75,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T00:00:00Z","timestamp":1788912000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T00:00:00Z","timestamp":1788912000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AI1684111"],"award-info":[{"award-number":["AI1684111"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DK138707"],"award-info":[{"award-number":["DK138707"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["GM152319"],"award-info":[{"award-number":["GM152319"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000015","name":"U.S. Department of Energy","doi-asserted-by":"publisher","award":["SC0015662"],"award-info":[{"award-number":["SC0015662"]}],"id":[{"id":"10.13039\/100000015","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["GM113132"],"award-info":[{"award-number":["GM113132"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["CA023108"],"award-info":[{"award-number":["CA023108"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["1S10OD030242"],"award-info":[{"award-number":["1S10OD030242"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DK117469"],"award-info":[{"award-number":["DK117469"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2026,9,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Strains of food-derived microbes can become facultative pathogens in susceptible human hosts. Surprisingly, we previously isolated\n                      <jats:italic toggle=\"yes\">Debaryomyces hansenii<\/jats:italic>\n                      , a yeast common in fermented foods, from Crohn disease (CD) ulcers, raising questions about its strain-specific traits that influence host interactions. Here, we further developed the genetic tractability of\n                      <jats:italic toggle=\"yes\">D. hansenii<\/jats:italic>\n                      and identified a single adhesin, Hil1, as a major determinant of colony morphology, biofilm formation, and immune targeting in CD patients. We used\n                      <jats:italic toggle=\"yes\">Agrobacterium tumefaciens<\/jats:italic>\n                      -mediated transformation to perform a forward genetic screen in a food-derived reference strain. We isolated mutants that converted from a wrinkled, biofilm-forming phenotype to a smooth, non-adherent phenotype characteristic of CD patient isolates. Mapping of multiple insertion sites showed a disrupted subtelomeric Hyr\/Iff-like adhesin gene, herein referred to as\n                      <jats:italic toggle=\"yes\">HIL1<\/jats:italic>\n                      . CRISPR-Cas9-mediated deletion of\n                      <jats:italic toggle=\"yes\">HIL1<\/jats:italic>\n                      recapitulated the mutant phenotype, demonstrating that\n                      <jats:italic toggle=\"yes\">HIL1<\/jats:italic>\n                      was necessary for biofilm formation and high cell-surface hydrophobicity phenotypes. To contextualize these findings, we performed comparative genomics on a\n                      <jats:italic toggle=\"yes\">D. hansenii<\/jats:italic>\n                      strain collection to assess allelic variation in the number of\n                      <jats:italic toggle=\"yes\">HIL1<\/jats:italic>\n                      tandem repeats. Longer alleles in food strains correlated with increased biofilm formation, while CD-isolated strains contained shorter\n                      <jats:italic toggle=\"yes\">HIL1<\/jats:italic>\n                      alleles and reduced binding to surfaces. Serology profiling showed that\n                      <jats:italic toggle=\"yes\">HIL1<\/jats:italic>\n                      was a direct antigenic target of circulating immunoglobulin G (IgG) in CD patients. Together, these results suggest Hil1 is a key, strain-variable adhesin shaping fungal surface properties and host immune recognition. This work establishes\n                      <jats:italic toggle=\"yes\">D. hansenii<\/jats:italic>\n                      as a genetically tractable system and shows how adhesin polymorphisms may influence fungal behavior in food and disease contexts.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Debaryomyces hansenii<\/jats:italic>\n                      is a yeast that is common in food and is generally recognized as safe for human consumption, though recently it has been identified within diseased regions of the intestine in Crohn disease patients. A current need is to determine the genetic and phenotypic differences between safe food isolates and isolates from human Crohn disease patient ulcers. Here, we used a loss-of-function genetic screen and identified\n                      <jats:italic toggle=\"yes\">HIL1<\/jats:italic>\n                      , an adhesin that we found mediates cellular adhesion in many food strains but not in patient strains. We identified circulating\n                      <jats:italic toggle=\"yes\">HIL1<\/jats:italic>\n                      -reactive antibodies in patients with Crohn disease, indicating that food strains can be a target of host immune responses through Hil1.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.01107-26","type":"journal-article","created":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T13:01:15Z","timestamp":1785416475000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["The role of\n                    <i>HIL1<\/i>\n                    in strain-level adhesion and immune recognition in\n                    <i>Debaryomyces hansenii<\/i>"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4226-718X","authenticated-orcid":true,"given":"Kevin 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