Fire blight (FB), caused by the Gram-negative bacterium Erwinia amylovora is a dangerous disease on pome fruit, including apple. The FB-susceptible cultivar ÔIdaredÕ was crossed with the resistant wild species clone Malus · robusta 5. A segregating population of 146 progeny has been tested by artificial shoot inoculation for susceptibility to FB. Progeny were infected from 0% to 100% of the shoot length. To identify chromosomal regions or loci responsible for resistance to FB of Malus · robusta 5, a set of microsatellite markers (simple sequence repeat, SSRs) was chosen covering all linkage groups of apple. Up to eight different microsatellites were bulked to one mutliplex PCR using four different labels and a fifth label for a size standard. Fifty-nine microsatellite markers out of 72 SSRs were polymorphic. Fifty-four of 66 loci detected could be mapped and were useful for the detection of related resistant loci. Alleles of microsatellites Hi03d06, CH03g07 and CH03e03 originating from the resistant donor M. robusta were associated with resistance to Erwinia amylovora. Up to eighty percent of the phenotypic variation could be explained by the interval spanned by SSRs CH03g07 and CH03e03, indicating the presence of a major resistance gene. All three microsatellites are located on the distal part of linkage group 3, spanning 15 cM. The SSR marker CH03e03 can be regarded as diagnostic marker for FB resistance. Only seven progeny expressing allele b (184 bp) of CH03e03 showed blighted shoot lengths of more than 30% and only nine progeny lacking allele b showed blighted shoot lengths of <30%. By setting a threshold of 30% shoot necrosis for resistance to FB, the 146 individuals segregate into 71 susceptible and 75 resistant plants, and resistance to FB maps 9 cM away from marker CH03e03.

The Fusarium mycotoxin deoxynivalenol (DON) facilitates fungal spread within wheat tissue and the development of Fusarium head blight disease. The ability of wheat spikelets to resist DON-induced bleaching is genotype-dependent. In wheat cultivar (cv.) CM82036 DON resistance is associated with a quantitative trait locus, Fhb1, located on the short arm of chromosome 3B. Gene expression profiling (microarray and real-time RT-PCR analyses) of DON-treated spikelets of progeny derived from a cross between cv. CM82036 and the DON-susceptible cv. Remus discriminated ten toxin-responsive transcripts associated with the inheritance of DON resistance and Fhb1. These genes do not exclusively map to Fhb1. Based on the putative function of the ten Fhb1-associated transcripts, we discuss how cascades involving classical metabolite biotransformation and sequestration processes, alleviation of oxidative stress and promotion of cell survival might contribute to the host response and defence against DON.

Resistance genes against Phytophthora infestans (Rpi genes), the most important potato pathogen, are still highly valued in the breeding of Solanum spp. for enhanced resistance. The Rpi genes hitherto explored are localized most often in clusters, which are similar between the diverse Solanum genomes. Their distribution is not independent of late maturity traits. This review provides a summary of the most recent important revelations on the genomic position and cloning of Rpi genes, and the structure, associations, mode of action and activity spectrum of Rpi and corresponding avirulence (Avr) proteins. Practical implications for research into and application of Rpi genes are deduced and combined with an outlook on approaches to address remaining issues and interesting questions. It is evident that the potential of Rpi genes has not been exploited fully.

Markers corresponding to 27 plant defense genes were tested for linkage disequilibrium with quantitative resistance to late blight in a diploid potato population that had been used for mapping quantitative trait loci (QTLs) for late blight resistance. Markers were detected by using (i) hybridization probes for plant defense genes, (ii) primer pairs amplifying conserved domains of resistance (R) genes, (iii) primers for defense genes and genes encoding transcriptional regulatory factors, and (iv) primers allowing amplification of sequences flanking plant defense genes by the ligation-mediated polymerase chain reaction. Markers were initially screened by using the most resistant and susceptible individuals of the population, and those markers showing different allele frequencies between the two groups were mapped. Among the 308 segregating bands detected, 24 loci (8%) corresponding to six defense gene families were associated with resistance at chi2 > or = 13, the threshold established using the permutation test at P = 0.05. Loci corresponding to genes related to the phenylpropanoid pathway (phenylalanine ammonium lyase [PAL], chalcone isomerase [CHI], and chalcone synthase [CHS]), loci related to WRKY regulatory genes, and other -defense genes (osmotin and a Phytophthora infestans-induced cytochrome P450) were significantly associated with quantitative disease resistance. A subset of markers was tested on the mapping population of 94 individuals. Ten defense-related markers were clustered at a QTL on chromosome III, and three defense-related markers were located at a broad QTL on chromosome XII. The association of candidate genes with QTLs is a step toward understanding the molecular basis of quantitative resistance to an important plant disease.