Plants are constantly being challenged by aspiring pathogens, but disease is rare. Why? Broadly, there are three reasons for pathogen failure. Either (1) the plant is unable to support the niche requirements of a potential pathogen and is thus a non? host; or (2) the plant possesses preformed structural barriers or toxic compounds that confine successful infections to specialized pathogen species; or (3) upon recognition of the attacking pathogen, defense mechanisms are elaborated and the invasion remains localized. All three types of interaction are said to be incompatible, but only the latter resistance mech? anism depends on induced responses. Successful pathogen invasion and disease (compatibility) ensue if the preformed plant defenses are inappropriate, the plant does not detect the pathogen, or the activated defense responses are ineffective. In this review, we examine the essential prerequisites for patho? gen recognition and the induction of localized defense responses. Preformed defenses are considered elsewhere in this issue (see Osbourn, 1996, in this issue). Race-specific pathogen recognition is hypothesized to re? sult from the direct or indirect interaction of the product of a dominant or semidominant plant resistance (R) gene with a product derived from the corresponding dominant pathogen avirulence (Avr) gene (Keen, 1992; Staskawicz et al., 1995). Subsequent signal transduction events are assumed to coordinate the activation of an array of defense responses. This "simple" model appears to explain much but begs many questions. For example, R gene products are likely to provide key components for recognition, but how do the distinct classes of R proteins characterized to date (see Bent, 1996, in this is? sue) activate the defense response? Do different R gene classes activate distinct responses? The regulation of some components of defense mechanisms has been studied in plant cell cultures in response to non-race-specific elicitors, but to what extent do such studies provide a model for R gene func? tion? Plant resistance is often correlated with the activation of specific defense responses, but which (if any) are required to abolish or retard pathogen growth, and how? Which are pri? mary responses and which are secondary? Does the first response involve transcriptional regulation, the activation of preformed enzymes, and/or the opening of ion channels, or

Resistance gene-dependent plant defense responses.

https://www.cell.com/cell/pdf/S0092-8674(00)81858-9.pdf

The Arabidopsis NPR1 gene that controls systemic acquired resistance encodes a novel protein containing ankyrin repeats

Arabidopsis mutants simulating disease resistance response

Rx-mediated extreme resistance against potato virus X in potato does not involve a necrotic hypersensitive response at the site of initial infection and thereby differs from the more usual type of disease resistance in plants. However, the Rx protein is structurally similar to products of disease resistance genes conferring the hypersensitive response. We show in both Nicotiana spp and potato that Rx has the potential to initiate a cell death response but that extreme resistance is separate and epistatic to necrosis. These data indicate that cell death and pathogen arrest are separate disease resistance responses in plants.

https://www.jstor.org/stable/pdfplus/3870814.pdf

The Rx Gene from Potato Controls Separate Virus Resistance and Cell Death Responses

The Arabidopsis EDS1 and PAD4 genes encode lipase-like proteins that function in resistance (R) gene-mediated and basal plant disease resistance. Phenotypic analysis of eds1 and pad4 null mutants shows that EDS1 and PAD4 are required for resistance conditioned by the same spectrum of R genes but fulfil distinct roles within the defence pathway. EDS1 is essential for elaboration of the plant hypersensitive response, whereas EDS1 and PAD4 are both required for accumulation of the plant defence-potentiating molecule, salicylic acid. EDS1 is necessary for pathogen-induced PAD4 mRNA accumulation, whereas mutations in PAD4 or depletion of salicylic acid only partially compromise EDS1 expression. Yeast two-hybrid analysis reveals that EDS1 can dimerize and interact with PAD4. However, EDS1 dimerization is mediated by different domains to those involved in EDS1–PAD4 association. Co-immunoprecipitation experiments show that EDS1 and PAD4 proteins interact in healthy and pathogen-challenged plant cells. We propose two functions for EDS1. The first is required early in plant defence, independently of PAD4. The second recruits PAD4 in the amplification of defences, possibly by direct EDS1–PAD4 association.

/pdf/direct-interaction-between-the-arabidopsis-disease-t3dxi33dnu.pdf

Direct interaction between the Arabidopsis disease resistance signaling proteins, EDS1 and PAD4

Peronospora parasitica causes downy mildew on crucifers. An isolate of P. parasitica (denoted NoCO2) was identified that infected Arabidopsis plants of the land race Columbia (Col-0) but not plants of land race Landsberg erecta (La-er). Segregation analysis of F2 plants derived from a La-er x Col-0 cross established that the resistance was inherited as a single locus, denoted RPP5. Macroscopic and microscopic examinations of inoculated La-er and Col-0 cotyledons showed that restriction of fungal growth in La-er was accompanied by massive callose accumulation and death of plant cells in direct contact with points of attempted fungal penetration. La-er x Col-0 F1 plants exhibited an intermediate resistance response in all aspects of fungal development, indicating that RPP5 is semi-dominant in its action. F8 recombinant inbred lines generated between La-er and Col-0 were used to map RPP5 to a narrow interval (<1.1 cM) on chromosome 4, utilizing existing restriction fragment length polymorphic (RFLP) markers and newly generated random amplified polymorphic DNA (RAPD) markers. The data provide a basis for the isolation of the RPP5 locus by positional cloning as a first step towards understanding recognitional specificity in plant-pathogen interactions at a molecular level.

https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-313X.1993.04050821.x

Veronique Szabo

Papers

Phenotypic characterization and molecular mapping of the Arabidopsis thaliana locus RPP5, determining disease resistance to Peronospora parasitica