Abstract
Sporulation efficiency in the yeast Saccharomyces cerevisiae is a well-established model for studying quantitative traits. A variety of genes and nucleotides causing different sporulation efficiencies in laboratory, as well as in wild strains, has already been extensively characterised (mainly by reciprocal hemizygosity analysis and nucleotide exchange methods). We applied a different strategy in order to analyze the variation in sporulation efficiency of laboratory yeast strains. Coupling classical quantitative genetic analysis with simulations of phenotypic distributions (a method we call phenotype modelling) enabled us to obtain a detailed picture of the quantitative trait loci (QTLs) relationships underlying the phenotypic variation of this trait. Using this approach, we were able to uncover a dominant epistatic inheritance of loci governing the phenotype. Moreover, a molecular analysis of known causative quantitative trait genes and nucleotides allowed for the detection of novel alleles, potentially responsible for the observed phenotypic variation. Based on the molecular data, we hypothesise that the observed dominant epistatic relationship could be caused by the interaction of multiple quantitative trait nucleotides distributed across a 60--kb QTL region located on chromosome XIV and the RME1 locus on chromosome VII. Furthermore, we propose a model of molecular pathways which possibly underlie the phenotypic variation of this trait.
Highlights
Phenotypic variation of complex, quantitative traits is an important subject of research in modern biology and one particular model for investigating such traits is sporulation efficiency in the yeast Saccharomyces cerevisiae
Coupling classical quantitative genetic analysis with simulations of phenotypic distributions enabled us to obtain a detailed picture of the quantitative trait loci (QTLs) relationships underlying the phenotypic variation of this trait
Based on the molecular data, we hypothesise that the observed dominant epistatic relationship could be caused by the interaction of multiple quantitative trait nucleotides distributed across a 60-kb QTL region located on chromosome XIV and the RME1 locus on chromosome VII
Summary
Phenotypic variation of complex, quantitative traits is an important subject of research in modern biology and one particular model for investigating such traits is sporulation efficiency in the yeast Saccharomyces cerevisiae. Yeast cells undergo sporulation when environmental conditions are not suitable for mitotic growth due to nitrogen starvation and/or a change in cellular respiration, caused by both an absence of a fermentable carbon source and the presence of a nonfermentable carbon source, such as acetate [1] This two-staged process, consisting of meiosis and spore morphogenesis, results in four spores encapsu-. The genotype-phenotype correlation is usually tested via functional analysis generally comprising of reciprocal hemizygosity analysis (RHA), allelic exchange methods and site-directed mutagenesis [5,6,7] Using these approaches, Deutschbauer et al [6] managed to pinpoint three nucleotide variants (associated with genes RME1, MKT1 and TAO3) which account for >90 % of the difference in sporulation between the low-sporulating strain S288c and high-sporulating strain SK1 of S. cerevisiae. The abundance of identified variants provides an excellent framework for correlating sporulation efficiencies of different yeast strains with specific gene and nucleotide compositions of the QTLs detected by these studies
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