Abstract
Concepts and procedures are presented for the analysis of progeny trials that incorporate clonal replication as a means to resolve variance arising from nonadditive gene effects. Components of variance from the linear model may be expressed in terms of expected covariances among relatives, and these, in turn, may be used to derive approximations of additive, dominance, and epistatic components of genetic variance. In addition to the usual assumptions applied to conventional progeny trials, the use of this expanded genetic model in the analysis of tests with clonal replicates assumes that the greatest portion of the total epistasis is due to interactions involving groups of more than two or three loci. If this assumption is not satisfied, estimates of additive and dominance variance, including those from trials without clonal replicates, will be contaminated by a large fraction of epistasis, and total epistasis will be underestimated by a corresponding amount. Heritability and gain formulae for alternative selection and deployment schemes are developed and illustrate the use of genetic parameters in the comparison of seedling and clonal reforestation strategies.

This publication has 0 references indexed in Scilit: