Resistance of Plants to Infectious Agents

Kuć, J.

doi:10.1146/annurev.mi.20.100166.002005

Cited by 71 publications

(27 citation statements)

References 95 publications

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“…This type of resistance is known as hypersensitive resistance (28,58,70,138). Hypersensitive resistance depends upon the plant's ability to respond sufficiently quickly to the presence of a pathogen such that the pathogen cannot penetrate past the fi rst cell or few cells of the plant with which it comes in contact.…”

Section: Varietal Specificity In Host-pathogen Systemsmentioning

confidence: 99%

“…This rapid response of the plant involves the death or sacrifi ce of the fi rst host cell(s) invaded, and thus the term hypersensitive response or hypersensitive resistance. These hypersensitive cells are the cells that produce molecules which either kill or at least prevent the further growth of the pathogen (13,28,58,70,78,83,118,119,138). mating type will specifically agglutinate cells of the opposite mating type (128,141).…”

Section: Varietal Specificity In Host-pathogen Systemsmentioning

confidence: 99%

“…Among the myriad microorganisms, viruses, nematodes, and insects that plants are exposed to, there are relatively few to which any plant is susceptible (28,70). Thus very effective mechanisms of general resistance enable plants to remain healthy in the face of potential attack by an enormous variety of pests.…”

Section: A Introductionmentioning

confidence: 99%

“…Thus very effective mechanisms of general resistance enable plants to remain healthy in the face of potential attack by an enormous variety of pests. General resistance must be based on mechanisms that are effective against a large number of different species of potential pathogens and pests (28,58,70,138).…”

Section: A Introductionmentioning

confidence: 99%

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Carbohydrates, Proteins, Cell Surfaces, and the Biochemistry of Pathogenesis

Albersheim¹,

Anderson-Prouty²

1975

Annu. Rev. Plant. Physiol.

242

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Section: Varietal Specificity In Host-pathogen Systemsmentioning

confidence: 99%

Section: Varietal Specificity In Host-pathogen Systemsmentioning

confidence: 99%

Section: A Introductionmentioning

confidence: 99%

Section: A Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Carbohydrates, Proteins, Cell Surfaces, and the Biochemistry of Pathogenesis

Albersheim¹,

Anderson-Prouty²

1975

Annu. Rev. Plant. Physiol.

242

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“…The resistance of a host plant to a parasite involves many mechanisms (see Kuc, 1966 ;CRUICKSHANK, 1966) . It is not logical to attribute all of such mechanisms to the function of one gene only .…”

Section: The Evolution Of Polygenes and Major Genes For Resistancementioning

confidence: 99%

The concept of breeding for uniform and differential resistance and their integration

Abdalla

Hermsen

1971

Euphytica

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It has been reported why resistance is needed in crop plants, how it has been searched for, and how long the resistance could be maintained in the host varieties . Uniform and differential resistance have been discussed and integrated within one genetic system . The possible evolution of both polygenes and major genes for resistance is discussed . Polygenes probably are `older' and produce the `materials' necessary for a host to show resistance, major genes acting as switching genes . Breeding for disease resistance has been briefly debated in connection with the discussion on host resistance .

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Pathological Changes in Ultrastructure: Effects of Victorin on Oat Roots

Hanchey

Wheeler

Luke

1968

American J of Botany

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Cells in the interior of susceptible oat roots treated with the disease‐inducing agent victorin exhibit many of the ultrastructural features which characterize the epidermal or outermost root cap cells of untreated roots. An increase in electron density of cell walls fixed in permanganate is the first effect of victorin seen in the root interior. Other early victorin‐induced changes are formation of enlarged, densely stained vesicles by the Golgi apparatus and organization of the endoplasmic reticulum into roughly parallel profiles. All of these features are characteristic of untreated epidermal cells. Victorin also induces the formation of large numbers of lomasome‐like wall lesions and causes a marked increase in the number of nearly spherical, membrane‐bounded structures tentatively identified as spherosomes. Similar lomasome‐ and spherosome‐like structures are much more abundant in the outermost cells of the root cap than in other regions of untreated roots. This suggests that these structures may be characteristic of cells destined to undergo disintegration. Victorin‐induced lesions appear to arise within the cell wall as the result of an activation of wall‐degrading enzymes. An early change which makes the unit structure of the plasma membrane visible over extended areas may account for victorin‐induced changes in permeability. Disrupted plasma membranes and swollen mitochondria are found only in cells heavily damaged by victorin. Many of the effects of victorin resemble those of calcium deficiency and calcium is known to suppress victorin‐induced disease symptoms. This suggests that calcium nutrition may play a role in the pathological changes induced by victorin.

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Resistance of Plants to Infectious Agents

Cited by 71 publications

References 95 publications

Carbohydrates, Proteins, Cell Surfaces, and the Biochemistry of Pathogenesis

Carbohydrates, Proteins, Cell Surfaces, and the Biochemistry of Pathogenesis

The concept of breeding for uniform and differential resistance and their integration

Pathological Changes in Ultrastructure: Effects of Victorin on Oat Roots

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