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Disruptions in the tRNA modification machinery, especially of the anticodon stem loop, can be lethal for many bacteria and lead to a broad range of phenotypes in baker\u2019s yeast. Very little is known about the function of tRNA modifications in host-pathogen interactions, where rapidly changing environments and stresses require fast adaptations. We found that two closely related fungal pathogens of humans, the highly pathogenic\n              <jats:italic>Candida albicans<\/jats:italic>\n              and its much less pathogenic sister species,\n              <jats:italic>Candida dubliniensis<\/jats:italic>\n              , differ in the function of a tRNA-modifying enzyme. This enzyme, Hma1, exhibits species-specific effects on the ability of the two fungi to grow in the hypha morphology, which is central to their virulence potential. We show that Hma1 has tRNA-threonylcarbamoyladenosine dehydratase activity, and its deletion alters ribosome occupancy, especially at 37\u00b0C\u2014the body temperature of the human host. A\n              <jats:italic>C. albicans HMA1<\/jats:italic>\n              deletion mutant also shows defects in adhesion to and invasion into human epithelial cells and shows reduced virulence in a fungal infection model. This links tRNA modifications to host-induced filamentation and virulence of one of the most important fungal pathogens of humans.\n            <\/jats:p>\n            <jats:sec>\n              <jats:title>IMPORTANCE<\/jats:title>\n              <jats:p>\n                Fungal infections are on the rise worldwide, and their global burden on human life and health is frequently underestimated. Among them, the human commensal and opportunistic pathogen,\n                <jats:italic>Candida albicans,<\/jats:italic>\n                is one of the major causative agents of severe infections. Its virulence is closely linked to its ability to change morphologies from yeasts to hyphae. Here, this ability is linked\u2014to our knowledge for the first time\u2014to modifications of tRNA and translational efficiency. One tRNA-modifying enzyme, Hma1, plays a specific role in\n                <jats:italic>C. albicans<\/jats:italic>\n                and its ability to invade the host. This adds a so-far unknown layer of regulation to the fungal virulence program and offers new potential therapeutic targets to fight fungal infections.\n              <\/jats:p>\n            <\/jats:sec>\n          <\/jats:sec>","DOI":"10.1128\/spectrum.04255-22","type":"journal-article","created":{"date-parts":[[2024,4,8]],"date-time":"2024-04-08T13:19:52Z","timestamp":1712582392000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":9,"title":["A highly conserved tRNA modification contributes to\n            <i>C. albicans<\/i>\n            filamentation and virulence"],"prefix":"10.1128","volume":"12","author":[{"given":"Bettina","family":"B\u00f6ttcher","sequence":"first","affiliation":[{"name":"Department of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology \u2013 Hans Knoell Institute, Jena, Germany"},{"name":"Septomics Research Center, Friedrich Schiller University and Leibniz Institute for Natural Product Research and Infection Biology \u2013 Hans Knoell Institute, Jena, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandra D.","family":"Kienast","sequence":"additional","affiliation":[{"name":"Max Planck Research Group for RNA Biology, Max Planck Institute for Molecular Biomedicine, M\u00fcnster, Germany"},{"name":"Research Group for Cellular RNA Biochemistry, Department of Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern, Bern, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Leufken","sequence":"additional","affiliation":[{"name":"Max Planck Research Group for RNA Biology, Max Planck Institute for Molecular Biomedicine, M\u00fcnster, Germany"},{"name":"Research Group for Cellular RNA Biochemistry, Department of Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern, Bern, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristian","family":"Eggers","sequence":"additional","affiliation":[{"name":"Max Planck Research Group for RNA Biology, Max Planck Institute for Molecular Biomedicine, M\u00fcnster, Germany"},{"name":"Research Group for Cellular RNA Biochemistry, Department of Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern, Bern, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Puneet","family":"Sharma","sequence":"additional","affiliation":[{"name":"Max Planck Research Group for RNA Biology, Max Planck Institute for Molecular Biomedicine, M\u00fcnster, Germany"},{"name":"Research Group for Cellular RNA Biochemistry, Department of Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern, Bern, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine M.","family":"Leufken","sequence":"additional","affiliation":[{"name":"Max Planck Research Group for RNA Biology, Max Planck Institute for Molecular Biomedicine, M\u00fcnster, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bianka","family":"Morgner","sequence":"additional","affiliation":[{"name":"Department of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology \u2013 Hans Knoell Institute, Jena, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannes C. 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