Abstract
To date, studies of the molecular basis of disease resistance mainly focused on qualitative resistance. However, deciphering mechanisms underlying quantitative resistance could lead to insights into the relationship between qualitative and quantitative resistance and guide the utilization of these two types of resistance to produce durably resistant cultivars. A functional genomics approach, using the CATMA whole-genome microarray, was used to detect changes in gene expression associated with partial quantitative resistance in the Arabidopsis thaliana–Plasmodiophora brassicae pathosystem. The time course of transcript abundance during partial clubroot resistance response was monitored at the whole plant level, and direct comparisons between partial resistance and susceptibility responses were made using the same host genotype. An increasingly complex host response was revealed, as was the differential influence of P. brassicae infection on the transcription of Arabidopsis genes according to the isolate used. We observed, at the transcriptomic level, that metabolic diversion by the pathogen was reduced or delayed, classical plant defense responses were induced earlier and/or more strongly, and cell enlargement and proliferation were actively inhibited in the partial quantitative resistance response compared to the susceptible one.Electronic supplementary materialThe online version of this article (doi:10.1007/s10142-013-0312-9) contains supplementary material, which is available to authorized users.
Highlights
Clubroot, caused by the obligate biotrophic protist Plasmodiophora brassicae Woron., is one of the most important diseases of Brassica crops, causing annual losses of 10– 15 % worldwide (Dixon 2009)
A set of differential hosts, including susceptible and resistant genotypes of different Brassica species, was evaluated at 49 dpi to characterize the isolate’s pathogenicity. This confirmed that both isolates, eH and e2 (Fähling et al 2003), used in this study belong to the P. brassicae pathotype P1 (Somé et al 1996)
The identification of genes regulated in partial clubroot resistance responses represents a major challenge for understanding the basis of partial quantitative resistance
Summary
Clubroot, caused by the obligate biotrophic protist Plasmodiophora brassicae Woron., is one of the most important diseases of Brassica crops, causing annual losses of 10– 15 % worldwide (Dixon 2009). The combination of adapted cropping practices as well as chemical and biological control methods is a feasible strategy for the management of clubroot in Brassica (reviewed in Donald and Porter 2009); plant resistance is still the most powerful tool for combating clubroot disease (Diederichsen et al 2009). Defined as a compatible host–pathogen interaction, partial resistance does limit the extent of the disease, either by rate-limiting pathogen multiplication or by reducing symptom severity This form of resistance, frequently under polygenic control, is important for crop improvement and can be selected, often constituting an additional layer of resistance in the absence of R-mediated resistance and leading to high levels of phenotypic resistance (Poland et al 2009). Because it is controlled by multiple genes with small effects (leading to lower selection pressure on the pathogen) and/or is presumed to have a broader specificity, quantitative resistance should be overcome more slowly by the pathogen and appears to be an alternative for the development of durable host plant resistance (Boyd 2006; Brun et al 2010; Palloix et al 2009)
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