
Dominant Epistasis between Two Quantitative Trait Loci Governing Sporulation Efficiency in Yeast Saccharomyces cerevisiae
Author(s) -
Juraj Bergman,
Petar Tomev Mitrikeski,
Krunoslav Brčić-Kostić
Publication year - 2015
Publication title -
food technology and biotechnology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.744
H-Index - 67
eISSN - 1334-2606
pISSN - 1330-9862
DOI - 10.17113/ftb.53.04.15.3998
Subject(s) - quantitative trait locus , epistasis , biology , genetics , phenotype , saccharomyces cerevisiae , gene , locus (genetics) , allele , genetic analysis , trait , chromosome , computer science , programming language
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.