Abstract
The potential infection biology of Plasmodiophora brassicae in resistant hosts and non-hosts is still not completely understood. Clubroot resistance assay on European clubroot differentials (ECD) set revealed that ECD10 (Brassica napus) and ECD4 (Brassica rapa) show a complete resistance to the tested P. brassicae isolate in contrast to highly susceptible hosts Westar (B. napus) and ECD5 (B. rapa). Previously, we used fluorescent probe-based confocal microscopy (FCM) to refine the life cycle of P. brassicae and indicate the important time points during its infection in Arabidopsis. Here, we used FCM to systematically investigate the infection of P. brassicae in two resistant host species ECD10 and ECD4 and two non-host crops wheat and barley at each indicated time points, compared with two susceptible hosts Westar and ECD5. We found that P. brassicae can initiate the primary infection phase and produce uninucleate primary plasmodia in both resistant hosts and non-hosts just like susceptible hosts at 2 days post-inoculation (dpi). Importantly, P. brassicae can develop into zoosporangia and secondary zoospores and release the secondary zoospores from the zoosporangia in resistant hosts at 7 dpi, comparable to susceptible hosts. However, during the secondary infection phase, no secondary plasmodium was detected in the cortical cells of both resistant hosts in contrast to massive secondary plasmodia present in the cortex tissue of two susceptible hosts leading to root swelling at 15 dpi. In both non-host crops, only uninucleate primary plasmodia were observed throughout roots at 7 and 15 dpi. Quantitative PCR based on DNA revealed that the biomass of P. brassicae has no significant increase from 2 dpi in non-host plants and from 7 dpi in resistant host plants, compared to the huge biomass increase in susceptible host plants from 2 to 25 dpi. Our study reveals that the primary infection phase in the root epidermis and the secondary infection phase in the cortex tissue are, respectively, blocked in non-hosts and resistant hosts, contributing to understanding of cellular and molecular mechanisms underlying clubroot non-host and host resistance.
Highlights
Clubroot disease, caused by the soil-borne protist pathogen Plasmodiophora brassicae, spreads over 60 countries and results in huge yield and economic losses worldwide (Dixon, 2014)
Plants of all European clubroot differentials (ECD) accessions were inoculated with resting spores of P. brassicae and evaluated for clubroot resistance at 25 dpi when plant roots of susceptible accessions B. rapa ECD5 and B. napus Westar showed severe clubroot symptoms (Figure 1)
For B. rapa accessions, all roots of ECD1 or ECD4 were club-free and free of gall showed a complete resistance against the P. brassicae isolate used in this study (Figure 1 and Supplementary Table S1)
Summary
Clubroot disease, caused by the soil-borne protist pathogen Plasmodiophora brassicae, spreads over 60 countries and results in huge yield and economic losses worldwide (Dixon, 2014). One important feature of P. brassicae is the pathogenic specialization which could be determined by various sets of clubroot differential hosts (Ayers, 1957; Williams, 1966; Buczacki et al, 1975; Somé et al, 1996; Strelkov et al, 2018). The Williams clubroot differential set (WCD) and European clubroot differential set (ECD) have been widely employed to determine the pathotypes of P. brassicae worldwide, and 7 pathotypes in China, 6 pathotypes in Canada, 8 pathotypes in France, and 23 pathotypes in Australia have been identified (Manzanares-Dauleux et al, 2001; Donald et al, 2006; Chai et al, 2014; Strelkov et al, 2018). WCD or ECD per se provides important resistant resources for Brassica crop resistance breeding and probing into resistance mechanism
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