Hypersensitivity

The coat protein of tobamovirus acts as elicitor of both L 2 and L 4 gene-mediated resistance in Capsicum

“…The hypersensitive response (HR) is a generalized active response in plants against pathogens (Klement, 1982;Goodman & Novacky, 1994), resulting in rapid cell death and restriction of pathogen growth at the site of infection. Usually the HR is a highly specific event that depends on a matching specificity between a disease resistance gene (R) in the plant and an avirulence gene (avr) in the pathogen, a concept referred to as gene-for-gene resistance (Flor, 1971).…”

Virulence of the Phytopathogen Pseudomonas syringae pv. Maculicola Is rpoN Dependent

“…hrp genes are required not only for pathogenicity of a virulent pathogen but also for the elicitation of the hypersensitive response (HR) which occurs on some hosts (44,45). The HR involves rapid, but localized, programmed plant cell death and is believed to restrict pathogen spread (1,37). There is mounting evidence that the elicitation of an HR is mediated by the specific interaction between the products of a plant resistance gene (R gene) and a pathogen avirulence (avr) gene (43,80,85).…”

Ensnaring microbes: the components of plant disease resistance

“…Parallels between this plant cell death phenotype and the programmed, apoptotic, cell death observed in other eukaryotes (Martin, 1993;Collins & Rivas, 1993), have been suggested (Lamb, 1994), However, the first detailed histological study undertaken specifically to address this equation using a non-host bacterially induced HR on lettuce to Pseudomonas syringae pv, phaseolicola, found no evidence to indicate that the plant cells underwent apoptosis (Bestwick, Bennett & Mansfield, 1995), But as this was non-host mediated HR it could be distinct from race-specific R-Avrmediated HR, The HR might only be a consequence of other rapidly induced defence responses, for example the oxidative burst or elevated lipoxygenase activity which eventually overcome the cellular protection mechanisms of cells within a certain distance from the original challenge site. Indeed, in several plant-pathogen interactions, if the environmental conditions are modified, for example by increasing humidity levels, microbial arrest can occur in the absence of HR (Klement, 1982;Hammond-Kosack & Jones, 1995). Similarly, the activation of numerous defence responses is still evident in the absence of HR (Jakobek & Lindgren, 1993).…”

“…Elevated SA levels can also inhibit wound-induced proteinase-inhibitor (pin) gene expression by blocking the activity of the key enzyme, hydroxyperoxide dehydrase, in jasmonic acid (JA) biosynthesis (Pena-Cortes et al, 1993), JA is required for the expression of several wound-inducible genes (Earmer, 1994), Thus at the site of i^-microbial incompatibility, elevated levels of SA should ensure that defence responses required to arrest microbial growth are activated, whereas those against chewing insects and migrating nematodes are not induced unnecessarily, A hypersensitive or rapid celi death response (HR) often accompanies the resistance response in many incompatible plant-microbe interactions (Klement, 1982), In suspension cultures, cell death is only evident after R gene-expressing lines are challenged with avirulent bacteria, but not after challenge with either race-specific or non-specific elicitors (Matthysse, 1987;Vera-Estrella et aL, 1992;Levme et al, 1994;Nurnberger et aL, 1994;Baker & Orlandi, 1995), In plants,, the localized collapse of cells during the HR is thought to deprive biotrophic microbes of nutrients, Eor necrotrophs, cellular decompartmentalisation might lead to the release upon the invader of harmful preformed substances, termed phytoanticipins (Van Etten et aL, 1994), or newly synthesized antimicrobial metabolites, termed phytoalexins (Darvill & Albersheim, 1984), stored in both the vacuole and cytoplasm. Alternatively, signals from the dying or dead host cells could induce an array of defence responses in the surrounding host cells and thereby localize the infection.…”

“…It is hypothesized that this recognition results from the direct or indirect interaction of the product of a dominant or semidominant plant resistance (K) gene with the product from the corresponding dominant pathogen .avirulence (Avr) gene (Flor, 1971;Keen, 1990;Dangl, 1995a;Staskawicz et al, 1995). Subsequent signal transduction events co-ordinate the resistance phenotype which includes the generation of active oxygen species, ion fluxes across membranes, changes in protein phosphorylation, transcriptional activation of plant defence-related genes, the rapid death of host cells around the penetration site (the hypersensitive response, HR) (Klement, 1982;Bowles, 1990;Dixon, Harrison & Lamb, 1994; and sometimes the induction of systemic acquired resistance . Only a limited number of signalling pathways may be required to initiate defence via R gene product action because similar types of plant defence responses are induced by very diverse microbes (Lamb, 1994;Dangl, 1995 a).…”