The genetic architecture of thermal tolerance and correlated growth-related traits in rainbow trout, Oncorhynchus mykiss
The localisation of variance for fitness-related traits to specific chromosomal regions may elucidate the underlying system of the genetic control of quantitative traits, potentially permitting selection on these traits. General linear modeling of allele inheritance at molecular marker loci was used to detect the presence and nature of quantitative trait loci (QTL) in two commercial strains of rainbow trout ('Oncorhynchus mykiss ') controlling variation in three traits: upper thermal tolerance (UTT), length (fork length, FL) and condition factor (residual fatness). Genetic variation was surveyed on three autosomes (linkage groups B, D and S) and the sex chromosomes (linkage group 18). One autosomal and one sex-linked QTL with major-moderate effects (7-10%) on UTT (on linkage groups S and 18, respectively) were detected, although QTL effects accounted for 1.5-10.0% of phenotypic variance. The existence of these QTL was determined both by testing associations between alleles inherited by progeny (i) from parents and (ii) from their grandsires. A sex-linked QTL for FL was also detected, suggesting pleiotropy or linkage disequilibrium among QTL for FL and UTT on the sex chromosomes. Physiological epistasis, the interactive effect of specific combinations of loci on phenotype, was highly locus-specific, with epistasis between genes on linkage groups B and 18 accounting for the majority of the cases in which epistatic effects were detected for all three traits, but particularly for UTT. In tests for physiological epistasis, females were more phenotypically divergent from their full and half sib family mean phenotype than males. Parental effects on UTT and size traits were detected in embryonic rainbow trout, indicating heritable variance for these traits. While autosomal UTT QTL on linkage groups B, S and 18 did not appear to affect UTT in embryonic rainbow trout, QTL affecting body length and weight at this stage were detected on linkage groups S and B. Physiological epistasis between genes on linkage group S and 18 on embryo length was extremely strong in one half sib family (r2 = 0.18; p < 0.0001). My results were suggestive of polygenic control of these traits (by numerous QTL), operating within a Wrightian framework, with physiological epistasis strongly influenced by sex-linked genes.