Background: Susceptibility to Fusarium wilt disease varies among wild accessions of Arabidopsis thaliana. Six RESISTANCE TO FUSARIUM OXYSPORUM (RFO) quantitative trait loci (QTLs) controlling the resistance of accession Columbia-0 (Col-0) and susceptibility of Taynuilt-0 to Fusarium oxysporum forma specialis matthioli (FOM) are detected in a recombinant population derived from a single backcross of the F1 hybrid (BC1). In particular, the RFO1 QTL appears to interact with three other loci, RFO2, RFO4 and RFO6, and is attributed to the gene At1g79670.
Results: When resistance to FOM was mapped in a new BC(1) population, in which the loss-of-function mutant of At1g79670 replaced wild type as the Col-0 parent, RFO1's major effect and RFO1's interaction with RFO2, RFO4 and RFO6 were absent, showing that At1g79670 alone accounts for the RFO1 QTL. Resistance of two QTLs, RFO3 and RFO5, was independent of RFO1 and was reproduced in the new BC(1) population. In analysis of a third BC1 population, resistance to a second pathogen, F. oxysporum forma specialis conglutinans race 1 (FOC1), was mapped and the major effect locus RFO7 was identified.
Conclusions: Natural quantitative resistance to F. oxysporum is largely specific to the infecting forma specialis because different RFO loci were responsible for resistance to FOM and FOC1. The mapping of quantitative disease resistance traits in BC(1) populations, generated from crosses between sequenced Arabidopsis accessions, can be a routine procedure when genome-wide genotyping is efficient, economical and accessible.