Homothallic strains of Saccharomyces cerevisiae can switch from one mating type to the other as often as every cell division. The conversion of mating type alleles (from MATa to MATalpha or vice versa) depends on other, unexpressed copies of a or alpha information that can be transposed to MAT. Previously, "inconvertible" mutations within MATalpha and MATa have been described that block the excision of the MAT allele. In this paper we describe two cis-acting mutations that also impair mating type switching and lie very near, but outside, the MAT locus. Both "stuck" mutations, stk1 and stk2, diminish the efficiency of converting MATa to MATalpha to less than 10% of normal. The stk1 mutation also slightly reduces conversion of MATalpha to MATa, whereas stk2 has no discernible effect. Unlike the inconvertible MATalpha-inc and MATa-inc mutations within MAT, the stk mutations are not replaced by wild-type sequences after the "stuck" cells occasionally switch to the opposite mating type. Because these mutations are not "healed" by mating type conversions, they must lie in sequences outside of the transposable mating type information. These results indicate that the efficient replacement of MAT alleles depends on sequences both within and adjacent to the MAT locus. Among subclones of homothallic stk MATa strains, approximately 2% show "illegal" transpositions of mating type genes. In these colonies the silent copy of alpha information at the HMLalpha locus has been converted to a, without any change of MATa or the silent a copy at HMRa. Such conversions of the unexpressed library genes are not found in wild-type homothallic strains that can switch mating type efficiently, but they are found in MATa-inc and MATalpha-inc strains. It appears that all of the cis-acting mutations within or adjacent to mating type result in these unusual switches of mating type information at HML and HMR.
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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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