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dc.contributor.authorKo, Hui-Chingen_US
dc.contributor.authorHsiao, Ting-Yinen_US
dc.contributor.authorChen, Chiung-Tongen_US
dc.contributor.authorYang, Yun-Liangen_US
dc.date.accessioned2014-12-08T15:31:24Z-
dc.date.available2014-12-08T15:31:24Z-
dc.date.issued2013-06-01en_US
dc.identifier.issn1225-8873en_US
dc.identifier.urihttp://dx.doi.org/10.1007/s12275-013-2577-zen_US
dc.identifier.urihttp://hdl.handle.net/11536/22318-
dc.description.abstractWe previously showed that the expression of ENO1 (enolase) in the fungal pathogen Candida albicans is critical for cell growth. In this study, we investigate the contribution of the ENO1 gene to virulence. We conducted our functional study of ENO1 in C. albicans by constructing an eno1/eno1 null mutant strain in which both ENO1 alleles in the genome were knockouted with the SAT1 flipper cassette that contains the nourseothricin-resistance marker. Although the null mutant failed to grow on synthetic media containing glucose, it was capable of growth on media containing yeast extract, peptone, and non-fermentable carbon sources. The null mutant was more susceptible to certain antifungal drugs. It also exhibited defective hyphal formation, and was avirulent in BALB/c mice.en_US
dc.language.isoen_USen_US
dc.subjectenolaseen_US
dc.subjectopportunistic human pathogenen_US
dc.subjectdrug susceptibilityen_US
dc.subjecthyphal formationen_US
dc.subjectvirulenceen_US
dc.titleCandida albicans ENO1 null mutants exhibit altered drug susceptibility, hyphal formation, and virulenceen_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s12275-013-2577-zen_US
dc.identifier.journalJOURNAL OF MICROBIOLOGYen_US
dc.citation.volume51en_US
dc.citation.issue3en_US
dc.citation.spage345en_US
dc.citation.epage351en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.department分子醫學與生物工程研究所zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.contributor.departmentInstitute of Molecular Medicine and Bioengineeringen_US
dc.identifier.wosnumberWOS:000321134100012-
dc.citation.woscount1-
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