QTL analysis of resistance to fusarium root rot in bean

A major constraint to dry edible and snap bean (Phaseolus vulgaris L.) production worldwide is root rot, one form of which is caused by Fusarium solani f. sp. phaseoli (Burk.) Snyd. & Hans (FSP). Sources of resistance to this pathogen exist in P. vulgaris, and, in the current paper, we studied the inheritance of one such source, FR266, using two recombinant inbred populations, MF and IF, derived from crosses of susceptible cultivars Montcalm (M) and Isles (T) with FR266 (F). Random amplified polymorphic DNA (RAPD) markers, associated with quantitative trait loci (QTL) controlling resistance to Fusarium root rot, also were identified. Genetic resistance to FSP, originally derived from PI 203958, was polygenically controlled and strongly influenced by environmental factors. Heritability estimates (h(2))were moderate and ranged from 0.48 to 0.71 for MF population. Several RAPD markers were identified that demonstrated significant associations with resistance to FSP determined from both greenhouse and field evaluations. Markers associated with field ratings tended not to be associated with greenhouse ratings and vice versa, except for the P-700 marker which was significantly associated with both greenhouse and field data. Individual markers identified in this study did not explain more than 15% of the phenotypic variation for root rot resistance, whereas a combination of four markers explained 29% of the phenotypic variation for root rot ratings in the field. The two regions of the bean genome associated with root rot resistance corresponded to loci controlling the Pv pathogenesis-related proteins (PvPR). Mechanisms associated with host defense responses may be involved in resistance to FSP and selection directed towards enhancing these traits may allow for rapid improvement of resistance to Fusarium root rot in bean.