{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:32:09Z","timestamp":1787016729516,"version":"build-2736575974"},"reference-count":99,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T00:00:00Z","timestamp":1770768000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T00:00:00Z","timestamp":1770768000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"publisher","award":["214229_Z_18_Z"],"award-info":[{"award-number":["214229_Z_18_Z"]}],"id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DE022550"],"award-info":[{"award-number":["DE022550"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000268","name":"Biotechnology and Biological Sciences Research Council","doi-asserted-by":"publisher","award":["UKRI717"],"award-info":[{"award-number":["UKRI717"]}],"id":[{"id":"10.13039\/501100000268","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2026,2,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Candida albicans<\/jats:italic>\n                      causes severe mucosal and systemic infections, with hypha formation playing a key role in its virulence. Hyphal invasion via endocytosis is mediated predominantly through interactions between Als3p and the epidermal growth factor receptor (EGFR). Subsequent EGFR activation by candidalysin, a hyphal-secreted cytolytic peptide toxin encoded by the\n                      <jats:italic toggle=\"yes\">ECE1<\/jats:italic>\n                      gene, induces receptor signaling and immune responses. While EGFR ubiquitination critically regulates receptor trafficking and signaling, its involvement during\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      infection has remained unexplored. Here, we demonstrate that\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      induces EGFR ubiquitination, leading to altered trafficking and lysosomal degradation in an\n                      <jats:italic toggle=\"yes\">ECE1<\/jats:italic>\n                      - and\n                      <jats:italic toggle=\"yes\">ALS3<\/jats:italic>\n                      -dependent manner. This correlates with changes in EGFR ligand expression, adaptor recruitment, and protein ubiquitination in oral epithelial cells. In a mouse model of oropharyngeal candidiasis, wild-type\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">ece1<\/jats:italic>\n                      \u0394\/\u0394 and\n                      <jats:italic toggle=\"yes\">als3<\/jats:italic>\n                      \u0394\/\u0394 mutant strains were found to differentially regulate\n                      <jats:italic toggle=\"yes\">Egfr<\/jats:italic>\n                      expression, ubiquitin pathway-associated genes, and protein ubiquitination. Furthermore, conditional EGFR knockout was protective during infection. Together, our findings reveal that\n                      <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                      infection modulates the host ubiquitin system, including direct effects on EGFR, highlighting a novel aspect of host\u2013fungal interactions.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        <jats:italic toggle=\"yes\">Candida albicans<\/jats:italic>\n                        is a common fungal pathogen that causes both mucosal infections, such as thrush, and life-threatening systemic diseases. A key step in infection is the fungus invading epithelial tissues and activating the host epidermal growth factor receptor (EGFR). We discovered that\n                        <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                        alters how EGFR is regulated by inducing its ubiquitination, a modification that leads to receptor degradation. This process depends on two major fungal virulence factors: the adhesin Als3p and Ece1p, the polypeptide that contains the candidalysin toxin. The fungus also broadly increases protein ubiquitination in oral epithelial cells. In a mouse model of oral infection, loss of EGFR in epithelial tissues reduced disease severity, suggesting that the receptor helps the fungus establish infection. These findings reveal a previously unrecognized strategy by which\n                        <jats:italic toggle=\"yes\">C. albicans<\/jats:italic>\n                        manipulates protein ubiquitination and regulation in epithelial cells, offering new insights into fungal pathogenesis and potential therapeutic approaches that target host pathways.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.03448-25","type":"journal-article","created":{"date-parts":[[2026,1,12]],"date-time":"2026-01-12T14:01:10Z","timestamp":1768226470000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["<i>Candida albicans<\/i>\n                    -induced ubiquitination of EGFR reveals novel host\u2013fungal interaction pathways"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-6221-7763","authenticated-orcid":true,"given":"L\u00e9a","family":"Lortal","sequence":"first","affiliation":[{"name":"Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King\u2019s College London","place":["London, United Kingdom"]},{"name":"Department of Biochemistry and Biophysics, University of California San Francisco","place":["San Francisco, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James S.","family":"Griffiths","sequence":"additional","affiliation":[{"name":"Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King\u2019s College London","place":["London, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily L.","family":"Priest","sequence":"additional","affiliation":[{"name":"Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King\u2019s College London","place":["London, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Kempf","sequence":"additional","affiliation":[{"name":"Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King\u2019s College London","place":["London, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivia K. A.","family":"Paulin","sequence":"additional","affiliation":[{"name":"Department of Molecular Genetics, University of Toronto","place":["Toronto, Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole O.","family":"Ponde","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01an3r305","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Rheumatology and Clinical Immunology, University of Pittsburgh","place":["Pittsburgh, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antzela","family":"Tsavou","sequence":"additional","affiliation":[{"name":"Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King\u2019s College London","place":["London, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Don N.","family":"Wickramasinghe","sequence":"additional","affiliation":[{"name":"Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King\u2019s College London","place":["London, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Donkin","sequence":"additional","affiliation":[{"name":"Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King\u2019s College London","place":["London, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claire M.","family":"Lyon","sequence":"additional","affiliation":[{"name":"Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King\u2019s College London","place":["London, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivia W.","family":"Hepworth","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases, Columbia University","place":["New York, 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A Nasab SDS Bidkhori G Vaga S Begum N Blagojevic M Singh N Griffiths J Kotowicz N Guennec AL Henley-Smith R Clasen F Miranda P Karimpour N Cook R Richardson J Thavaraj S Naglik J Shoaie S Moyes D. 2022. Fungal infection drives metabolic reprogramming in epithelial cells via aerobic glycolysis and an alternative TCA cycle shunt. 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