Series of gain-of-function missense mutations in PDR1 and PDR3 that encode transcription factors are known to increase the expression of ABC transporters that extrude various kinds of drugs out of a cell, leading to pleiotropic drug resistance (PDR). Previously, the PDR1-H176 (L309S) allele from a clotrimazole (CTZ)-resistant sake yeast mutant has been cloned and found to be sufficient to confer PDR and improved fermentative activity on the arginase-deficient (car1/car1) sake yeast HL163. In this study, another PDR1 and three PDR3 a!leles were cloned from other CTZ-resistant mutants. These alleles contain different missense mutations, PDR1-2 (M308I), PDR3-C21 (L950S), PDR3-C231 (G948D), and PDR3-11 (G957D). The gene recombinants containing each of the mutations found in CTZ-resistant mutants were constructed using the wild-type sake yeast K1001. The gene recombination was designed to generate only a nucleotide replacement without any other DNA changes such as insertion of external DNA fragments. The resultant recombinants that were heterozygous for each of the mutations showed various degrees of drug resistance that were comparable to those of the CTZ-resistant mutants. The recombinants, except one introduced with PDR1-H176, also fermented sake mash faster and produced higher amounts of alcohol than K1001 did. These results demonstrated that PDR1-2, PDR3-C21, PDR3-C231, and PDR3-11 are sufficient to confer PDR and improved fermentative activity on K1001, and suggested that previous results in which fermentative activity of HL163 was significantly improved by PDR1-H176 must have depended on its genetic background, probably arginase deficiency.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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