We generated all possible haploid and homozygous diploid genotypes at 6 biosynthetic loci in yeast and scored their fitness to examine whether there was any pattern of weak synergistic epistasis, which is a requirement of the deterministic mutation model for the evolution of sex. We measured 4 components of fitness: haploid growth rate, haploid mating efficiency, diploid growth rate, and diploid sporulation efficiency. We found that in agreement with previous work in yeast, epistasis tended to be small in magnitude and variable in sign, regardless of the fitness component measured. The number of background mutations had either no effect or no consistent effect on epistasis distributions. For every combination of 2 loci in a mutation-free background, we also generated all heterozygous genotypes so that we could partition diploid epistasis into additive x additive, additive x dominance, and dominance x dominance epistasis. Our main interest was in determining whether dominance by dominance epistasis was large and negative, which is a requirement of diploid models with inbreeding to explain high levels of recombination. Dominance by dominance epistasis estimates obtained by partitioning diploid epistasis for growth rates were both positive and negative. With the caveat that our results are based on only 6 biosynthetic loci, epistasis for fitness is not supported as an explanation for the maintenance of sex or the high rate of meiotic recombination in yeast.
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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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