B.P.H.J. Thomma

Concomitant Activation of Jasmonate and Ethylene Response Pathways Is Required for Induction of a Plant Defensin Gene in Arabidopsis

Activation of the plant defensin gene PDF1.2 in Arabidopsis by pathogens has been shown previously to be blocked in the ethylene response mutant ein2-1 and the jasmonate response mutant coi1-1. In this work, we have further investigated the interactions between the ethylene and jasmonate signal pathways for the induction of this defense response. Inoculation of wild-type Arabidopsis plants with the fungus Alternaria brassicicola led to a marked increase in production of jasmonic acid, and this response was not blocked in the ein2-1 mutant. Likewise, A. brassicicola infection caused stimulated emission of ethylene both in wild-type plants and in coi1-1 mutants. However, treatment of either ein2-1 or coi1-1 mutants with methyl jasmonate or ethylene did not induce PDF1.2, as it did in wild-type plants. We conclude from these experiments that both the ethylene and jasmonate signaling pathways need to be triggered concomitantly, and not sequentially, to activate PDF1.2 upon pathogen infection. In support of this idea, we observed a marked synergy between ethylene and methyl jasmonate for the induction of PDF1.2 in plants grown under sterile conditions. In contrast to the clear interdependence of the ethylene and jasmonate pathways for pathogen-induced activation of PDF1.2, functional ethylene and jasmonate signaling pathways are not required for growth responses induced by jasmonate and ethylene, respectively.

The complexity of disease signaling in Arabidopsis

Not more than 10 years ago it was generally accepted that pathogen-inducible defense mechanisms in plants are triggered through a central signaling cascade that regulates a multicomponent defense response. Now we know that the plant defense system is regulated through a complex network of various signaling cascades.

Alternaria spp.: from general saprophyte to specific parasite

UNLABELLED SUMMARY Alternaria species are mainly saprophytic fungi. However, some species have acquired pathogenic capacities collectively causing disease over a broad host range. This review summarizes the knowledge on pathogenic strategies employed by the fungus to plunder the host. Furthermore, strategies employed by potential host plants in order to ward off an attack are discussed. TAXONOMY Alternaria spp. kingdom Fungi, subkingdom Eumycotera, phylum Fungi Imperfecti (a non-phylogenetic or artificial phylum of fungi without known sexual stages whose members may or may not be related; taxonomy does not reflect relationships), form class Hypomycetes, Form order Moniliales, form family Dematiaceae, genus Alternaria. Some species of Alternaria are the asexual anamorph of the ascomycete Pleospora while others are speculated to be anamorphs of Leptosphaeria. HOST RANGE Most Alternaria species are common saprophytes that derive energy as a result of cellulytic activity and are found in a variety of habitats as ubiquitous agents of decay. Some species are plant pathogens that cause a range of economically important diseases like stem cancer, leaf blight or leaf spot on a large variety of crops. Latent infections can occur and result in post-harvest diseases or damping-off in case of infected seed. Useful Website:

Disease development of several fungi on Arabidopsis can be reduced by treatment with methyl jasmonate

Abstract Pretreatment of Arabidopsis plants with gaseous methyl jasmonate (MeJA) caused efficient reduction of disease development by either the necrotrophic fungi Alternaria brassicicola, Botrytis cinerea or Plectosphaerella cucumerina. Protection by gaseous MeJA was also observed on the salicylic acid (SA)-degrading transformant NahG and the ethylene non-responsive mutant ein2-1, but not on the jasmonate non-responsive mutant coi1-1. In general, protection conferred by spraying with a MeJA solution was much lower compared to exposure to gaseous MeJA. 2,6-Dichloroisonicotinic acid (INA), a compound that activates SA- but not JA-dependent defence responses, failed to cause protection against either A. brassicicola or B. cinerea. On the other hand, INA treatment was efficient in reducing disease development by P. cucumerina.

Design and development of a DNA array for rapid detection and identification of multiple tomato vascular wilt pathogens

Fusarium wilt, caused by Fusarium oxysporum f. sp. lycopersici, and Verticillium wilt, caused by either Verticillium albo-atrum or Verticillium dahliae, are devastating diseases of tomato (Lycopersicon esculentum) found worldwide. Monitoring is the cornerstone of integrated pest management of any disease. The lack of rapid, accurate, and reliable means by which plant pathogens can be detected and identified is one of the main limitations in integrated disease management. In this paper, we describe the development of a molecular detection system, based on DNA array technology, for rapid and efficient detection of these vascular wilt pathogens. We show the utility of this array for the sensitive detection of these pathogens from complex substrates like soil, plant tissues and irrigation water, and samples that are collected by tomato growers in their greenhouses.

Quantification of disease progression of several microbial pathogens on Arabidopsis thaliana using real‐time fluorescence PCR

An accurate monitoring of disease progression is important to evaluate disease susceptibility phenotypes. Over the years, Arabidopsis thaliana has become the model species to serve as a host in plant-pathogen interactions. Despite the efforts to study genetic mechanisms of host defense, little efforts are made for a thorough pathogen assessment, often still depending on symptomology. This manuscript describes the use of real-time polymerase chain reaction (PCR) to assess pathogen growth in the host Arabidopsis for a number of frequently studied pathogens. A wide range of correlations between pathogen biomass and fluorescence is demonstrated, demonstrating the theoretical sensitivity of the technique. It is also demonstrated that host DNA does not interfere with the quantification of pathogen DNA over a wide range. Finally, quantification of pathogen biomass in different plant genotypes with a varying degree of resistance shows the capability of this technique to be used for assessment of pathogen development in disease progression.

Different micro-organisms differentially induce Arabidopsis disease response pathways

In the model plant Arabidopsis thaliana, several signal transduction pathways can be activated upon pathogen challenge leading to the activation of different (sets of) effector molecules. In the past it has been demonstrated that these different signal transduction pathways contribute differentially to resistance against distinct microbial pathogens. In this study, it is shown that not all pathogens activate the full set of defence responses. This indicates that depending on the particular interactions between elicitors and suppressors with their cognate plant targets, defence response cascades may or may not become activated during pathogenesis. These findings imply that current models of plant-pathogen interactions must be revised to take into account the pathogen-dependent nature of many defence responses.

The jasmonate-insensitive mutant jin1 shows increased resistance to biotrophic as well as necrotrophic pathogens

SUMMARY Jasmonic acid and related oxylipin compounds are plant signalling molecules that are involved in the response to pathogens, insects, wounding and ozone. To explore further the role of jasmonates in stress signal transduction, the response of two jasmonate-signalling mutants, jin1 and jin4, to pathogens and ozone was analysed in this study. Upon treatment with the biotrophic bacterial pathogen Pseudomonas syringae, endogenous jasmonate levels increased in jin1 and jin4 similar to wild-type, demonstrating that these mutants are not defective in jasmonate biosynthesis. Jin1 but not jin4 is more resistant to P. syringae and this higher resistance is accompanied by higher levels of salicylic acid. Jin1 is also more resistant to the necrotrophic fungal pathogen Botrytis cinerea and shows wild-type sensitivity to ozone whereas jin4 is more susceptible to B. cinerea and ozone. These results indicate that the mutations in jin1 and jin4 affect different branches of the jasmonate signalling pathway. Additionally, in this combination of phenotypes, jin1 is unique among all other jasmonate-related mutants described thus far. These data also provide support for a crosstalk between the jasmonate and salicylate pathways.

Tissue-specific expression of plant defensin genes PDF2.1 and PDF2.2 in Arabidopsis thaliana

Abstract Plant defensins are a family of cysteine-rich peptides, many members of which have been shown to exhibit antimicrobial activity. Sequence analysis of randomly expressed sequence tags has revealed the presence of five different plant defensin genes in Arabidopsis thaliana . Previous work has established the tissue-specific expression pattern of PDF1.1, PDF1.2 and PDF2.3 . The present study reports on the expression patterns of PDF2.1 and PDF2.2 . A compilation of all available data indicates that all Arabidopsis organs constitutively express one, and most of them two or more, plant defensin genes. Expression of PDF1.2 is upregulated upon infection of leaves by a fungal pathogen, while that of PDF2.2 is downregulated.

The Arabidopsis mutant iop1 exhibits induced over-expression of the plant defensin gene PDF1.2 and enhanced pathogen resistance.

SUMMARY Jasmonate and ethylene are concomitantly involved in the induction of the Arabidopsis plant defensin gene PDF1.2. To define genes in the signal transduction pathway leading to the induction of PDF1.2, we screened for mutants with induced over-expression of a beta-glucuronidase reporter, under the control of the PDF1.2 promoter. One mutant, iop1 (induced over-expressor of PDF1.2) produced small plants that showed induced over-expression of the pathogenesis-related genes PR-3, PR-4 and PR-1,2 (PDF1.2), combined with a down-regulated induction of PR-1 upon pathogen inoculation. The iop1 mutant showed enhanced resistance to a number of necrotrophic pathogens.