Genetic Analysis of Resistance to Pythium Ultimum a Major Component of Replant Disease in Apple Rootstocks

Abstract

Apple rootstocks from the Geneva® breeding program tolerated apple replant disease in experimental and commercial plantings in North and South America, Europe and Africa. Apple replant disease (ARD) is biological in nature and composed of several fungal, oomycete and nematode actors that when combined can stunt or even kill young roots. A major contributor to the ARD syndrome is the necrotrophic soilborne oomycete Pythium ultimum, which can individually overwhelm young roots and root hairs causing them to decline. Genetic resistance to ARD and its components has been incorporated into apple rootstocks from a wild apple species Malus x robusta‘Robusta 5’. This research was aimed at increasing our understanding of the genetic complexity of the resistance to P. ultimumin progeny of ‘Robusta 5’. In a replicated experiment we phenotyped 48 individual progeny (breeding lines) belonging to a larger population derived from a cross between replant susceptible apple rootstock ‘Ottawa 3’ and resistant ‘Robusta 5’. We also leveraged existing genomic infrastructure in the form of high-density genetic maps composed of microsatellite and single nucleotide polymorphic markers segregating in the same cross. When combined with the genotypic means of the 48 progeny in Quantitative Trait Locus (QTL) analysis, candidate genomic locations were identified on chromosomes 2, 5, 13, 16 and 17 that were associated with relative susceptibility of those breeding lines to P. ultimuminfection. The allelic effects of the loci were measured using a generalized linear model and their combinatorial interactions were studied. Of the resistance allelic effects examined all but one were derived from ‘Robusta 5’. The ultimate goal of this work is to develop genetic markers that can aid in the selection of P. ultimumresistant rootstocks. However, the multi-locus nature of this resistance trait may necessitate that only loci with larger effects (on chromosome 5, 17 and 13) be targeted for further development.