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Fungal cell growth and function requires ATP, which is synthesized mainly through oxidative phosphorylation, with the key enzyme being F<jats:sub>1<\/jats:sub>F<jats:sub>o<\/jats:sub>-ATP synthase. Here, we show that deletion of the <jats:italic>Candida albicans<\/jats:italic> gene encoding the \u03b4 subunit of the F<jats:sub>1<\/jats:sub>F<jats:sub>o<\/jats:sub>-ATP synthase (<jats:italic>ATP16<\/jats:italic>) abrogates lethal infection in a mouse model of systemic candidiasis. The deletion does not substantially affect in vitro fungal growth or intracellular ATP concentrations, because the decrease in oxidative phosphorylation-derived ATP synthesis is compensated by enhanced glycolysis. However, the <jats:italic>ATP16<\/jats:italic>-deleted mutant displays decreased phosphofructokinase activity, leading to low fructose 1,6-bisphosphate levels, reduced activity of Ras1-dependent and -independent cAMP-PKA pathways, downregulation of virulence factors, and reduced pathogenicity. A structure-based virtual screening of small molecules leads to identification of a compound potentially targeting the \u03b4 subunit of fungal F<jats:sub>1<\/jats:sub>F<jats:sub>o<\/jats:sub>-ATP synthases. The compound induces in vitro phenotypes similar to those observed in the <jats:italic>ATP16<\/jats:italic>-deleted mutant, and protects mice from succumbing to invasive candidiasis. Our findings indicate that F<jats:sub>1<\/jats:sub>F<jats:sub>o<\/jats:sub>-ATP synthase \u03b4 subunit is required for <jats:italic>C. albicans<\/jats:italic> lethal infection and represents a potential therapeutic target.<\/jats:p>","DOI":"10.1038\/s41467-021-26313-9","type":"journal-article","created":{"date-parts":[[2021,10,15]],"date-time":"2021-10-15T15:30:38Z","timestamp":1634311838000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["The \u03b4 subunit of F1Fo-ATP synthase is required for pathogenicity of Candida albicans"],"prefix":"10.1038","volume":"12","author":[{"given":"Shuixiu","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yajing","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yishan","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanli","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhanpeng","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chuanyan","family":"Tang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luobei","family":"Weng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaohong","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1917-0283","authenticated-orcid":false,"given":"Gehua","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5063-4082","authenticated-orcid":false,"given":"Hong","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,10,15]]},"reference":[{"key":"26313_CR1","unstructured":"Fungal disease frequency (GAFFI, 2017); Available at https:\/\/www.gaffi.org\/why\/fungal-disease-frequency\/. 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