A New
            <i>Helminthosporium</i>
            Blight of Oats

Meehan, Frances; Murphy, H. C.

doi:10.1126/science.104.2705.413

Cited by 104 publications

(43 citation statements)

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“…62,63 While (hemi)biotrophs have evolved strategies to suppress HR, some necrotrophs use the plant HR machinery as a strategy to promote virulence. 64 The necrotrophic fungus Cochliobolus victoriae, originally described as the causal agent of Victoria blight in oats, 65 secretes the toxin Victorin, required for pathogenicity. 66 This fungus hijacks HR via activation of a CC-NB-LRR protein LOV1, which confers sensitivity to victorin and susceptibility to C. victoriae in Arabidopsis.…”

Section: Pathogen Strategies To Evade Cell Deathmentioning

confidence: 99%

Programmed cell death in the plant immune system

2011

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Cell death has a central role in innate immune responses in both plants and animals. Besides sharing striking convergences and similarities in the overall evolutionary organization of their innate immune systems, both plants and animals can respond to infection and pathogen recognition with programmed cell death. The fact that plant and animal pathogens have evolved strategies to subvert specific cell death modalities emphasizes the essential role of cell death during immune responses. The hypersensitive response (HR) cell death in plants displays morphological features, molecular architectures and mechanisms reminiscent of different inflammatory cell death types in animals (pyroptosis and necroptosis). In this review, we describe the molecular pathways leading to cell death during innate immune responses. Additionally, we present recently discovered caspase and caspase-like networks regulating cell death that have revealed fascinating analogies between cell death control across both kingdoms.

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Section: Pathogen Strategies To Evade Cell Deathmentioning

confidence: 99%

Programmed cell death in the plant immune system

2011

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“…It is known to increase the cell membrane permeability of susceptible oat plants (Avena sativa), containing the Victoria (Vb) gene, which also encodes for resistance (Pc-2) against Puccinia coronata (16,31). Changes in membrane permeability were most typically expressed in irreversible K+ efflux from leaves, roots, and leaf protoplasts (2,12,18,24,30).…”

Section: Introductionmentioning

confidence: 99%

Electrical Membrane Properties of Leaves, Roots, and Single Root Cap Cells of Susceptible Avena sativa

Ullrich¹,

Novacký²

1991

Plant Physiol.

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The effect of the purified host-selective toxin victorin C, a cyclized penta peptide, was compared to that of CCCP and vanadate on membrane functions of susceptible leaves, roots, and single root cap cells of Avena sativa with conventional electrophysiology. The plasmalemma depolarized irreversibly by about 80 millivolts and to below the diffusion potential within 1 hour. Concentrations as low as 12.5 picomolar were effective in the susceptible but not the resistant cultivar. Electrical membrane potential difference changes were independent of pH and could not be prevented by fusicoccin or Ca2 . Membranes began to depolarize after a lag phase that never was shorter than 6.5 minutes, even with concentrations as high as 1.25 micromolar. Membrane depolarization was accompanied by a distinct decrease in specific membrane resistance from 4.5 to 1.0 ohm times square meter on average. These changes were followed by K+ and Cl-efflux and extracellular alkalinization. ATP level and 02 uptake did not decrease within 2 hours. It is concluded that the victorin-induced deleterious membrane alterations are not caused by direct interaction with the plasmalemma H+-ATPase, K+ channels, lipid structure, nor energy metabolism, but they seem to be triggered by a cascade of events leading to an unspecific increase in membrane permeability.Victorin C is a host-selective toxin, a cyclized penta peptide (32), produced by the phytopathogenic fungus Cochliobolus victoriae Nelson. It is known to increase the cell membrane permeability of susceptible oat plants (Avena sativa), containing the Victoria (Vb) gene, which also encodes for resistance (Pc-2) against Puccinia coronata (16,31). Changes in membrane permeability were most typically expressed in irreversible K+ efflux from leaves, roots, and leaf protoplasts (2,12,18,24,30). K+ efflux might be triggered by several mechanisms: (a) a direct or indirect (by stalling the energy supply) inhibition of the plasmalemma H+-ATPase and thus depolarization of the membrane and opening of the K+ channels; (b) an interaction with K+ channels; (c) a direct change in channel-unrelated unspecific membrane permeability by alteration 'Supported by the Deutsche Forschungsgemeinschaft (C. U.), by an Alexander von Humboldt Senior U.S. Scientist award, and by the National Science Foundation, DMB-8516038 (A. N.) 675 of the lipid structure or an indirect one via an intracellular sequence of events, starting with binding of the toxin to a specific membrane-located binding protein (31). The molecular mechanism, however, is still unknown.With K+ selective electrodes only flux changes beyond the nmol range can be detected. However, for a measurable change in the electrical membrane potential of plant cells, a charge transfer ofless than one pmol * cm-2 is required. Hence, measurements of membrane potential changes with conventional electrophysiological methods are at least 1000 times more sensitive in indicating changes in membrane properties than continuous K+ concentration measurements. To detect victor...

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“…Victoria blight of Avena sativa (oat) is caused by the necrotrophic fungus, Cochliobolus victoriae (Meehan and Murphy, 1946), which is pathogenic because of the production of the hostspecific toxin, victorin (Meehan and Murphy, 1947). Isolates of C. victoriae that produce victorin are pathogenic on susceptible A. sativa (Meehan and Murphy, 1947), whereas mutants or outcrosses that do not produce the toxin are nonpathogenic.…”

Section: Introductionmentioning

confidence: 99%

Purification and Characterization of Serine Proteases That Exhibit Caspase-Like Activity and Are Associated with Programmed Cell Death in Avena sativa

2004

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Victoria blight of Avena sativa (oat) is caused by the fungus Cochliobolus victoriae, which is pathogenic because of the production of the toxin victorin. The victorin-induced response in sensitive A. sativa has been characterized as a form of programmed cell death (PCD) and displays morphological and biochemical features similar to apoptosis, including chromatin condensation, DNA laddering, cell shrinkage, altered mitochondrial function, and ordered, substrate-specific proteolytic events. Victorin-induced proteolysis of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) is shown to be prevented by caspase-specific and general protease inhibitors. Evidence is presented for a signaling cascade leading to Rubisco proteolysis that involves multiple proteases. Furthermore, two proteases that are apparently involved in the Rubisco proteolytic cascade were purified and characterized. These proteases exhibit caspase specificity and display amino acid sequences homologous to plant subtilisin-like Ser proteases. The proteases are constitutively present in an active form and are relocalized to the extracellular fluid after induction of PCD by either victorin or heat shock. The role of the enzymes as processive proteases involved in a signal cascade during the PCD response is discussed.

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A New Helminthosporium Blight of Oats

Cited by 104 publications

References 0 publications

Programmed cell death in the plant immune system

Programmed cell death in the plant immune system

Electrical Membrane Properties of Leaves, Roots, and Single Root Cap Cells of Susceptible Avena sativa

Purification and Characterization of Serine Proteases That Exhibit Caspase-Like Activity and Are Associated with Programmed Cell Death in Avena sativa

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