Brown patch, caused by Rhizoctonia solani Kühn, is a devastating disease of tall fescue (Festuca arundinacea Schreb.). Developing genetic resistance is a viable long term control strategy; however, the genetic mechanism of brown patch resistance in tall fescue is not known. The objectives for this research were to (i) calculate the broad and narrow-sense heritability for brown patch resistance, (ii) determine the relative importance of additive and non-additive (dominance and epistatic) gene effects for brown patch resistance, (iii) estimate the general and specific combining abilities of tall fescue parents for brown patch resistance, (iv) estimate the minimum number of effective genes involved in brown patch resistance, and (v) develop a genetic linkage map and identify the presence of quantitative trait loci for brown patch resistance in tall fescue.To complete these objectives, several field trials were conducted to evaluate the resistance of a diverse background of tall fescue genotypes, as well as parents and progeny from controlled crosses after inoculation with R. solani. Expressed Sequence Tags Simple Sequence Repeats (EST-SSRs) along with genomic-SSR markers were used to develop a genetic linkage map of a mapping population derived from a cross between a resistant genotype and a susceptible genotype.iii Analysis of the phenotypic data indicated brown patch resistance in tall fescue is heavily influenced by the environment with phenotypic responses displaying a continuous distribution, both characteristics indicative of quantitative inheritance.Additive genetic variance was more important than non-additive genetic variance in brown patch resistance in tall fescue. It was estimated that one to three genes were segregating for resistance in the progeny that were evaluated. A genotypic recurrent selection program would be the most effective for improving brown patch resistance in tall fescue. Molecular marker analysis revealed the presence of two putative quantitative trait loci.iv ACKNOWLEDGEMENT
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