{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T15:16:07Z","timestamp":1787498167611,"version":"build-2736575974"},"update-to":[{"DOI":"10.1371\/journal.pgen.1012118","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T00:00:00Z","timestamp":1777420800000}}],"reference-count":53,"publisher":"Public Library of Science (PLoS)","issue":"4","license":[{"start":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T00:00:00Z","timestamp":1776729600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["210879364 C2"],"award-info":[{"award-number":["210879364 C2"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["210879364 Z2"],"award-info":[{"award-number":["210879364 Z2"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100008769","name":"University of W\u00fcrzburg","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100008769","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["www.plosgenetics.org"],"crossmark-restriction":false},"short-container-title":["PLoS Genet"],"abstract":"<jats:p>\n                    Protein kinases are key components of many signaling pathways that regulate cellular activities, and some of them are indispensable for the viability of cells. We used inducible gene deletion to assess the importance of a set of putative essential protein kinases for growth and viability of the pathogenic yeast\n                    <jats:italic>Candida albicans<\/jats:italic>\n                    and to get clues about the functions of uncharacterized essential kinases. We found that\n                    <jats:italic>bud32<\/jats:italic>\n                    \u0394,\n                    <jats:italic>ctk1<\/jats:italic>\n                    \u0394,\n                    <jats:italic>rio1<\/jats:italic>\n                    \u0394, and\n                    <jats:italic>rio2<\/jats:italic>\n                    \u0394 mutants were viable but grew very slowly, explaining previous failures to generate homozygous deletion mutants.\n                    <jats:italic>PTK2<\/jats:italic>\n                    was essential, but under certain conditions\n                    <jats:italic>ptk2<\/jats:italic>\n                    \u0394 mutants remained viable and over time could acquire suppressor mutations in the Ptk2-dependent plasma membrane ATPase Pma1 that restored growth. Deletion of the uncharacterized\n                    <jats:italic>orf19.5376<\/jats:italic>\n                    was lethal and the null mutants formed pseudohyphae that lacked normal septa and eventually lysed, a phenotype that was phenocopied by auxin-induced protein depletion. The mutants were defective in septin organization, indicating that the\n                    <jats:italic>orf19.5376<\/jats:italic>\n                    -encoded kinase is functionally similar to the nonessential kinase Elm1 of\n                    <jats:italic>Saccharomyces cerevisiae<\/jats:italic>\n                    , but is indispensable for viability in\n                    <jats:italic>C. albicans<\/jats:italic>\n                    . Mutants lacking\n                    <jats:italic>orf19.3456<\/jats:italic>\n                    , which does not have a homolog in\n                    <jats:italic>S. cerevisiae<\/jats:italic>\n                    , were also nonviable and grew as aseptate, sometimes multinucleate hyphae before cell death. Co-immunoprecipitation followed by liquid chromatography-mass spectrometry identified a protein, encoded by the uncharacterized\n                    <jats:italic>orf19.193<\/jats:italic>\n                    , as a candidate regulatory subunit of the\n                    <jats:italic>orf19.3456<\/jats:italic>\n                    -encoded kinase, as mutants lacking this protein exhibited the same terminal phenotype as\n                    <jats:italic>orf19.3456<\/jats:italic>\n                    mutants. These results provide strong evidence that instead of using a mitotic exit network (MEN) with only two kinases (Cdc15 and Dbf2), as was previously thought,\n                    <jats:italic>C. albicans<\/jats:italic>\n                    regulates septum formation and cytokinesis via a septation initiation network (SIN), known from fission yeast and filamentous fungi, which contains a protein kinase cascade consisting of the upstream kinase Cdc15, the\n                    <jats:italic>orf19.3456<\/jats:italic>\n                    -encoded kinase, and the downstream kinase Dbf2.\n                  <\/jats:p>","DOI":"10.1371\/journal.pgen.1012118","type":"journal-article","created":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T17:44:56Z","timestamp":1776793496000},"page":"e1012118","update-policy":"https:\/\/doi.org\/10.1371\/journal.pgen.corrections_policy","source":"Crossref","is-referenced-by-count":1,"title":["Inducible gene deletion reveals essentiality of protein kinases and 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