The Interaction of Plasmodiophora brassicae and Arabidopsis thaliana: Parameters for Disease Quantification and Screening of Mutant Lines

Abstract

The soil‐borne obligate pathogen Plasmodiophora brassicae causes clubroot disease in species of Brassicaceae, including Arabidopsis thaliana. The host–pathogen interaction was studied with respect to the age of the plant at the time point of inoculation and to different infection pressures in order to establish a standardization of infection parameters and evaluation of disease extent for A. thaliana lines. Spore number per root weight, root and shoot weight of inoculated and non‐inoculated plants as well as infection rate and disease index (DI) were analysed and correlated. The disease extent of different lines was comparable as measured by the relation of root weight of inoculated and non‐inoculated plants (Ri/Rni index) and the DI. Most of the 71 screened A. thaliana lines turned out to be susceptible. However, the mutant lines tu8, tu3, det1‐1, and rhd3‐1 showed a certain degree of tolerance under specific culture conditions. The reactions of rhd3‐1 indicate that hypertrophy is a prerequisite for maturation of the pathogen. The reactions of the tu3 and tu8 mutants indicate a role of indole glucosinolates and indole‐3‐acetonitrile/IAA in development of clubroot disease.

Analysis of global host gene expression during the primary phase of the Arabidopsis thaliana–Plasmodiophora brassicae interaction

“…Indeed, jasmonic acid may be acting as an antagonist of salicylic acid synthesis, as has been suggested by several researchers (Kunkel and Brooks 2002;Glazebrook et al 2003). The jar1 mutant was more sensitive to clubroot infection, according to Siemens et al (2002), and was also confirmed to be susceptible to the Australian population of P. brassicae. Induction of one lipoxygenase gene at 23 DAI has been shown by Siemens et al (2006), indicating a potential role for jasmonic acid during gall development (Ludwig-Müller and Schuller 2008).…”

“…As discussed in a recent review (LudwigMüller and Schuller 2008), according to the microarray analysis of Siemens et al (2006), several ethylene responsive genes were differentially expressed, clearly indicating a role for ethylene in clubroot development. Interestingly, the ethylene-resistant mutants (etr1-1 and etr1-3) and ethylene-insensitive mutants (ein3-1 and ein4) tested by Siemens et al (2002) did not show tolerance to clubroot. Resistance to P. brassicae infection was shown by Devos et al (2006) in the alh1 mutant defective in cross-talk between ethylene and auxin.…”

“…Broadly speaking, in resistant hosts, the primary phase of the lifecycle can still be observed, but not the secondary phase (Dekhuijzen 1979;Takahashi et al 2006;Donald et al 2008). In a compatible (susceptible) interaction with Arabidopsis thaliana (L.) Heynh., the pathogen can proceed through its entire lifecycle from 3 to 28 days, as studied by Siemens et al (2002). Recent work has demonstrated that P. brassicae attachment to, and penetration of, the root hair can occur from Day 4 after inoculation onwards (Agarwal et al 2009).…”

“…Furthermore, a review of the interactions of P. brassicae with its hosts (Ludwig-Müller and Schuller 2008) once again emphasised that although the components of early signalling in the interaction between A. thaliana and leaf pathogens are well understood, there are relatively few studies with root pathogens and indeed none conducted with P. brassicae. A comparative study between resistance and susceptibility is not possible for the interaction of P. brassicae with A. thaliana, as almost all the A. thaliana ecotypes tested so far are susceptible to P. brassicae (Siemens et al 2002;Agarwal et al 2009). Also, the enormous variation in the virulence of P. brassicae populations reported worldwide (Jones et al 1982) often makes it difficult to determine the host's genomic and metabolomic responses.…”

Variability in resistance to clubroot in European cauliflower cultivars

“…Plants were evaluated in the stage of having at least three true leaves in water, in order to assess the infection degree precisely. The modified disease index (DI) following Siemens et al (2002) was calculated according to the formula DI = (0n 0 + 1n 1 + 2n 2 + 2n 3 ) × 100/3N t where: n 0 -n 3 -number of plants in the indicated class N t -total number of plants tested…”