Contrasting mechanisms of defense against biotrophic and In contrast, necrotrophic pathogens benefit from host cell death, so they are not. Contrasting mechanisms of defense against Biotrophic and Necrotrophic Pathogens. Author: Glazebrook, J. Source: Annual review of phytopathology v Glazebrook, J. () Contrasting Mechanisms of Defense against Biotrophic and Necrotrophic Pathogens. Annual Review of Phytopathology, 43,
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The role of salicylic acid SA and jasmonic acid JA signaling in resistance to root pathogens has been poorly documented. We assessed the contribution of SA and JA to basal and partial resistance of Arabidopsis to the biotrophic clubroot agent Plasmodiophora brassicae. SA signaling was activated in Bur-0 but not in Col The JA pathway was weakly activated in Bur-0 but was strongly induced in Col The contribution of both pathways to clubroot resistance was then assessed using exogenous phytohormone application and mutants affected in SA or JA signaling.
Exogenous SA treatment decreased clubroot symptoms in the two Arabidopsis accessions, whereas JA treatment reduced clubroot symptoms only in Col The cpr mutant, in which SA responses are constitutively induced, was more resistant to clubroot than the corresponding wild type, and the JA signaling-deficient mutant jar1 was more susceptible. NATA1 and nata1 lines displayed reduced or enhanced clubroot symptoms, respectively, thus suggesting that in Col-0 this pathway was involved in the JA-mediated basal clubroot resistance.
Overall, our data support the idea that, depending on the Arabidopsis accession, both SA and JA signaling can play a role in partial inhibition of clubroot development in compatible interactions with P.
A large body of genetic and cellular studies on plant defense signaling have led to the general conceptual model in which different hormonal pathways tightly control specific plant responses toward pathogens with different lifestyles Thomma et al.
Even if at present this model is still being actively studied and was confirmed in some pathosystems Pieterse et al. For example, Glazebrook provided evidence that the JA pathway may help in defense against some biotrophs such as Peronospora parasitica and Erysiphe spp.
However, in contrast to the abundant literature on foliar pathogens, the biology of root defense against telluric pathogens has been less well studied Okubara and PaulitzBalmer and Mauch-ManiChen et al. In Arabidopsis thalianaJA- and SA-controlled responses in roots and their role in the orchestration of defenses have been described for only a few pathosystems.
Clubroot is a worldwide root disease affecting Brassicaceae species and caused by the obligate biotrophic soilborne Plasmodiophora brassicae. The life cycle of this pathogen comprises a primary phase restricted to the root hairs and a secondary phase of several weeks in cortical and stele cells.
During this secondary phase, the intracellular development of pathogen plasmodia causes cell hyperplasia and hypertrophia, and results in the formation of root galls Kageyama and Asano In this accession, JA accumulated in developing clubs Gravot et al.
Moreover, the jasmonate resistant mechanusms jar1 mutant, impaired in JA-Ile accumulation, exhibited heightened susceptibility to clubroot Agarwal et al. Abolition of the induction of arginase activity in the argah2 mutant line led to enhanced clubroot symptom development, thus providing further evidence for necrrotrophic role of the JA-dependent response in weak Col-0 basal resistance Gravot et al. This atypical amino acid has been reported to exert a negative effect on the reproduction of aphids Adio et al.
In addition to the above-described responses in Col-0, results from transcriptome analysis in Arabidopsis Jubault et al. These data suggested a paradoxical situation where infection by the same single isolate, virulent on the two genotypes Bur-0 and Col-0, would induce two different defense responses depending on the plant genotype. Bur-0 was described as partially resistant to eH Alix et al.
We thus hypothesized that SA- and JA-triggered defenses could drive contrasted levels of resistance in Bur-0 and Col-0, respectively. This assumption was, however, only based on the comparison of transcriptomic fingerprints and needed further investigation. The aim of the present study was therefore to obtain a more comprehensive view of SA- and JA-dependent root cellular responses to P.
PR1 expression remained at very low levels data not shown under all conditions. In the Bur-0 accession, however, infection induced a and fold increase in PR2 contrastlng PR5 expression, respectively, at 14 dpi.
Thereafter, at least for PR5the induction level was sustained at 17 dpi. Transcript levels of the SA-responsive genes PR2 A and PR5 B and SA accumulation C in infected black bars and non-infected roots white bars of the partially resistant accession Bur-0 and the susceptible accession Col-0 at 10, 14 and 17 dpi.
Error bars represent the SE 24 plants per block, six randomized blocks. SA accumulation was then paralleled with expression of these SA-responsive genes at 10, 14 and 17 dpi.
Biotrophic Fungi Infection and Plant Defense Mechanism | OMICS International
SA accumulation was not observed in Col-0 pf infection at any time point considered Fig. Thus, these results suggested that P. The expression of THI2. The infection induced the expression of THI2.
The same pattern of expression was observed for ARGAH2 ; the expression in Col-0 was four times higher at 14 dpi and twice as high at 17 dpi than in Bur However, JA accumulation was 2—3 times higher in Col-0 than in Bur-0 infected roots at each time point Fig. These results indicated that P. In contrast, in the partially resistant Bur-0, clubroot infection induced the SA pathway in the middle of the secondary phase of infection and then the JA pathway, but to a lesser extent biotrophi later stages.
The involvement of SA and JA in the response to clubroot was evaluated by exogenous application of these hormones. Clubroot symptoms were then quantified at 21 dpi. Non-treated inoculated Bur-0 plants exhibited fewer clubroot symptoms than Col-0, consistent with the previously reported partial resistance of Bur-0 Jubault et al. Exogenous SA treatment led to the decrease of clubroot symptoms in both Col-0 and Bur-0 bitorophic. In contrast, JA treatment reduced clubroot symptoms only in Col-0 Fig.
The relative amount of P. The results indicated that JA treatment reduced root pathogen density within infected roots of Col-0 and Bur-0 Fig. Despite the above-described effect of exogenous SA on symptom development, this treatment had no impact on pathogen density within root samples. A Illustration of clubroot symptoms of non-treated and treated Col-0 and Bur-0 accessions at 21 dpi. Error bars represent the SE 12 plants per block, four randomized blocks.
Error bars represent the SE pool of 12 plants per block, four randomized blocks. SA- and Deffnse genes and clubroot symptoms were then evaluated in a set defens mutants affected in SA conrtasting JA signaling during clubroot infection. Clubroot symptoms in the cpr mutant were 2-fold less severe than those of WT Col-0 Fig.
Clubroot symptoms were found to be clearly enhanced in biotropjic compared with Col-0, thus suggesting that JA responses contribute to clubroot resistance Fig. In the eds mutant, which is defective in SA accumulation, there was a small reduction in PR2 expression in infected roots compared with the WT Col-0 Fig.
This suggests that the eds5 mutation againt JA responses induced by P. Interestingly, clubroot symptoms were slightly reduced by the eds5 mutation Fig. NATA1 expression was highly induced by clubroot infection, but only in Col-0, where its expression was 40 times higher in inoculated vs.
In contrast, NATA1 was expressed at very low levels in both non-inoculated and inoculated Bur-0 roots. NATA1 Adio et al. Compared with the WT Col-0 backgroundnata1 was one-third more susceptible to clubroot, in contrast to 35S:: NATA1 which was one-third more resistant to clubroot Fig. The density of P. NATA1 mutants white bars. In this study, we aimed to investigate the involvement of Mecahnisms and JA pathways in mechanisma resistance of Arabidopsis to one compatible P.
Overall, our findings give a more detailed view of JA- and SA-triggered defenses induced by this pathogen in Arabidopsis roots. This study also suggests that both pathhogens pathways contribute to the inhibition of the post-invasive development of clubroot. The contribution of the SA and JA pathways to the resistance response appears to depend on the Arabidopsis accession considered. Indeed, differences in hormonal responses among Arabidopsis accessions, notably between Bur-0 and Col-0 Koornneef et al.
However, these observations were mostly made in leaves, and few data are available concerning the response at the root level. SA accumulation and the expression of the SA-responsive pathohens during clubroot agaainst are poorly documented. At the transcriptional level, Siemens et al. In the Bur-0 accession, the strong induction of PR2 and PR5 observed in this study agrees with the microarray results obtained by Jubault et al.
The absence of PR1 expression in both Col-0 and Bur-0 clubroot-infected roots agrees with the microarray results of Siemens et al. Interestingly, low levels of PR1 expression were reported in other root pathosystems, notably after challenging with Nwcrotrophic schachtii Wubben et al. The time-course induction of SA-related defenses in Bur-0 is consistent with a possible role for the SA pathway in limiting clubroot development during the secondary phase of infection.
The idea that SA responses can contribute to partial resistance was also supported by our hormone treatments and genetic approaches. Indeed, we showed that SA treatment had a protective effect against clubroot symptoms in both Arabidopsis accessions. In our work, however, the SA treatment did not modulate P. This result may suggest that symptom extent and pathogen density in infected tissues can be controlled by different factors.
The possible role of SA signaling in clubroot partial resistance was furthermore supported by the reduction of clubroot symptom development pathobens the cpr mutant. Previous defenze Bowling et al.
In our work, cpr infected by P. In contrast, the very low expression of THI2. Accordingly, clubroot ppathogens were similar in Col-0, npr and nahG. However, it was more difficult to explain the observed phenotype of the SA-deficient mutant edswhich exhibited slightly less symptoms than Col The eds mutant has been mainly characterized at the foliar level and showed reduced SA accumulation and no differences in the expression of PR2 pathogrns PR5 following P.
To our knowledge, induction of THI2. Thus the slight increase in clubroot resistance observed in the eds mutant could be associated with high expression of the JA-responsive gene THI2. These results would also suggest that EDS5 is involved in the partial down-regulation of the JA pathway in Arabidopsis roots.
MeJA treatment did not reduce clubroot symptoms in Bur We can therefore speculate that the endogenous clubroot-induced SA had an antagonistic effect on the exogenously applied MeJA. The antagonism between the two hormone pathways has been highlighted in several host—pathogen interactions Mur et al.
JA accumulation during clubroot infection was previously reported by Grsic et al.
Contrasting mechanisms of defense against biotrophic and necrotrophic pathogens.
The high JA levels observed during the secondary phase of infection in Chinese cabbage roots were similar to those we obtained in the biotrophc Col-0 accession. This is consistent with the microarray results of Siemens et al. These results suggested that root defense responses can diverge from leaf defense responses, as previously highlighted in different reports on hormone-treated or pathogen-challenged roots Edgar et al.
The lack of induced THI2.