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Here, we show that the human fungal pathogen\n                  <jats:italic>Cryptococcus neoformans<\/jats:italic>\n                  possesses two divergent Wee1-family kinases, CnSwe1 and CnSwe102, that retain conserved CDK-inhibitory activity but function differently from their counterparts in the canonical\n                  <jats:italic>Saccharomyces cerevisiae<\/jats:italic>\n                  morphogenesis checkpoint. The\n                  <jats:italic>swe1<\/jats:italic>\n                  \u0394 and\n                  <jats:italic>swe102<\/jats:italic>\n                  \u0394 mutants displayed distinct stress-response defects, and genetic analyses suggested a dosage-sensitive genetic interaction between\n                  <jats:italic>SWE1<\/jats:italic>\n                  and\n                  <jats:italic>SWE102<\/jats:italic>\n                  . Although both proteins promoted Cdc28 tyrosine phosphorylation and elongated-cell morphology when expressed in\n                  <jats:italic>S. cerevisiae<\/jats:italic>\n                  , neither localized to the mother-bud neck in\n                  <jats:italic>C. neoformans<\/jats:italic>\n                  . Altered\n                  <jats:italic>SWE1<\/jats:italic>\n                  dosage in the absence of\n                  <jats:italic>SWE102<\/jats:italic>\n                  increased sensitivity to replicative and DNA-damaging stresses and perturbed cell-cycle progression under genotoxic conditions. Importantly, loss of\n                  <jats:italic>SWE1<\/jats:italic>\n                  nearly abolished virulence in a murine infection model, and\n                  <jats:italic>SWE102<\/jats:italic>\n                  also contributed to pathogenicity. Together, these findings indicate that the conserved Wee1-CDK module acts in\n                  <jats:italic>C. neoformans<\/jats:italic>\n                  as a dosage-sensitive checkpoint that promotes stress adaptation and fungal virulence.\n                <\/jats:p>","DOI":"10.64898\/2026.06.24.734400","type":"posted-content","created":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T05:30:33Z","timestamp":1782451833000},"source":"Crossref","is-referenced-by-count":0,"title":["<i>Cryptococcus neoformans<\/i>\n                  rewires the conserved Wee1-CDK checkpoint through two divergent kinases required for replication-stress tolerance and virulence"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3077-1116","authenticated-orcid":false,"given":"Jin-Tae","family":"Choi","sequence":"first","affiliation":[{"name":"Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, South 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