{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,18]],"date-time":"2026-01-18T15:07:04Z","timestamp":1768748824438,"version":"3.49.0"},"reference-count":35,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2002,6,28]],"date-time":"2002-06-28T00:00:00Z","timestamp":1025222400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Microbiology"],"published-print":{"date-parts":[[2002,7]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Here, we report an indispensable role for spindle assembly checkpoint (SAC) component CaMad2p in the survival and virulence of <jats:italic>Candida albicans<\/jats:italic> in mice. We hypothesized that cell cycle checkpoint functions, especially those monitoring the integrity of DNA and chromosome segregation, might be required for the pathogen to repair damage caused by host defence. To test this idea, we created SAC\u2010defective mutants by deleting the <jats:italic>CaMAD2<\/jats:italic> gene that encodes a key component of the SAC pathway. The <jats:italic>CaMAD2<\/jats:italic> mutant appears normal in morphology, growth rate and growth mode switch in unperturbed conditions. However, it quickly loses viability when treated with nocodazole, which causes disassembly of mitotic spindles. The mutant also exhibits increased frequency of chromosome loss. The virulence of the mutant is greatly reduced in mice, presumably because of the inability of the mutant cells to stop the cell cycle when the host defence damages cellular components important for chromosome segregation. Supporting this hypothesis, unlike the wild\u2010type cells that can proliferate within and eventually grow out of macrophages, most of the <jats:italic>CaMAD2<\/jats:italic> null mutant cells are unable to survive. This study suggests that SAC is required for survival of <jats:italic>C. albicans<\/jats:italic> in the host and could thus be targeted for anti\u2010<jats:italic>C. albicans<\/jats:italic> therapies.<\/jats:p>","DOI":"10.1046\/j.1365-2958.2002.02995.x","type":"journal-article","created":{"date-parts":[[2003,3,12]],"date-time":"2003-03-12T11:44:30Z","timestamp":1047469470000},"page":"31-44","source":"Crossref","is-referenced-by-count":64,"title":["Spindle assembly checkpoint component CaMad2p is indispensable for <i>Candida albicans<\/i> survival and virulence in mice"],"prefix":"10.1111","volume":"45","author":[{"given":"Chen","family":"Bai","sequence":"first","affiliation":[]},{"given":"Narendrakumar","family":"Ramanan","sequence":"additional","affiliation":[]},{"given":"Yan Ming","family":"Wang","sequence":"additional","affiliation":[]},{"given":"Yue","family":"Wang","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[2002,6,28]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.1999.01641.x"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1101\/gr.148600"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1054\/tuld.1998.0200"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.25.13997"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)80875-2"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1084\/jem.177.6.1605"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1007\/s002940050181"},{"key":"e_1_2_6_9_1","doi-asserted-by":"crossref","first-page":"717","DOI":"10.1093\/genetics\/134.3.717","article-title":"Isogenic strain construction and gene mapping in Candida 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