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Hypersensitive Response
in plants
Dr. Joginder Pal Rao
Asstt. Prof., Plant Pathology
CSKHPKV Palampur
GN Agrios, 2005
Hypersensitive Resoponse in plants and defence
Hypersensitive Response- a mechanism used by plants, to
prevent spread of infection by microbial pathogens
Definition: The plant hypersensitive response (HR) is a
rapid localized cell death that occurs at the point of
pathogen penetration and is associated with disease
resistance.
or
• is a localized induced cell defense in the host plant at the
sites of infection by the pathogen.
• The hypersensitie response occurs only in specific host-
pathogen combinations in which host and the pathogen
are incombatible i.e. pathogen fails to infect the host
 E.C.Stakman, 1915 was the first to use the term
‘hypersensitive’ in plant pathology
Hypersensitive Resoponse in plants and defence
Hypersensitive Resoponse in plants and defence
Hypersensitive Resoponse in plants and defence
Hypersensitive Resoponse in plants and defence
• The hypersensitive response is the culmination of the plant
defense responses initiated by:
– the recognition by the plant of specific pathogen-produced signal
molecules, known as elicitors. Recognition of the elicitors by the host
plant activates a cascade of biochemical reactions in the attacked and
surrounding plant cells and
– leads to new or altered cell functions and to new or greatly activated
defense-related compounds
• The most common new cell functions and compounds include:
– a rapid burst of reactive oxygen species, leading to a dramatic increase
of oxidative reactions;
– increased ion movement, especially of K+ and H+ through the cell
membrane;
– disruption of membranes and loss of cellular compartmentalization
– production of antimicrobial substances such as phenolics
(phytoalexins); and formation of antimicrobial so-called pathogenesis-
related proteins such as chitinases.
• The HR is characterized by the rapid death of cells in the local region
surrounding an infection. The HR serves to restrict the growth and spread
of pathogens to other parts of the plant.
• The HR is analogous to the innate immune system found in animals, and
commonly precedes a slower systemic (whole plant) response, which
ultimately leads to systemic acquired resistance (SAR).
• Result in sudden death of the host cells in the vicinity of the pathogen
– Highest degree of resistance
• Both structural & biochemical in nature
• Common in obligate pathogens like fungi, viruses and nematodes, also
found in other fungal & bacterial infection
• Due to HR
– The necrotic tissues isolate the obligate pathogen from living cells.
– Devoid the pathogen of nutrition, thus starved and die.
• The HR is triggered by the plant when it recognizes a pathogen. The identification of a
pathogen typically occurs when virulence genes, secreted by a pathogen, bind to, or
indirectly interact with the product of a plant resistance (R) gene. Plant R genes are
highly polymorphic, and many plants produce several different types of R gene products,
enabling them to recognize virulence products produced by many different pathogens.
• In phase one of the HR, the activation of R genes triggers an ion flux, involving an efflux
of hydroxide and potassium outside the cells, and an influx of calcium and hydrogen ions
into the cell.
• In phase two, the cells involved in the HR generate an oxidative burst by producing
reactive oxygen species (ROS), superoxide anions, hydrogen peroxide, hydroxyl radicals
and nitrous oxide. These compounds affect cellular membrane function, in part by
inducing lipid peroxidation and by causing lipid damage.
• The alteration of ion components in the cell, and the breakdown of cellular components in
the presence of ROS, results in the death of affected cells and the formation of local
lesions. Reactive oxygen species also trigger the deposition of lignin and callose, as well
as the production of hydroxyproline-rich glycoproteins. These compounds serve to
reinforce the walls of cells surrounding the infection, creating a barrier and inhibiting the
spread of the infection.
Consequences of HR
 Depolarization of the membrane
 Electrolyte leakage
 Loss of selective membrane permeability
 Apposition of material to the cell wall
 Increased cytoplasmic streaming
 Translocation of nucleus to infection site
 Callose deposition and papillae formation
 Condensation of nucleoplasm and cytoplasm
 Disintegration of cytoskeleton
 Cleavage of nuclear DNA
 cells surrounding the lesion synthesize antimicrobial compounds,
including phenolics, phytoalexins, and pathogenesis related (PR)
proteins, including β-glucanases and chitinases
1. Non-host Resistance
• When a plant resist the attack of pathogenic organism which
is otherwise not the host of that pathogen is termed as non
host resistance
– e.g. potato late blight pathogen do not infect apple or
wheat plant and similarly apple pathogen like V.
inaequalis do not attack potato
• Similarly, the fungus that causes powdery mildew on wheat
(Blumeria (Erysiphe) graminis f. sp. tritici) does not infect
barley and vice versa, the fungus that causes powdery
mildew on barley (B. graminis f. sp. hordei) does not infect
wheat, and so on.
2. True resistance
• Disease resistance that is controlled
genetically by the presence of one, a few or
many genes for resistance in the plant is
known as true resistance
Types:
• Horizontal resistance
• Vertical resistance
Horizontal resistance:
• Also referred as partial, race non-specific
quantitative, Durable, Field, Minor gene,
polgenic or multigene resistance
Vertical resistance:
• Also known as strong, R-gene resistance,
Major gene resistance, Race specific,
Monogenic or oligogenic resistance
Cytoplasmic resistance
• In several plant diseases, resistance is controlled
by genetic material contained/present in the
cytoplasm of the cell. Such resistance is
sometimes referred to as cytoplasmic resistance.
• The two best examples of cytoplasmic resistance
occur in the Southern corn leaf blight caused by
Bipolaris (Helminthosporium) maydis and the
Yellow leaf blight caused by Phyllosticta
3. Apparent Resistance
• Under certain conditions or circumstances, some susceptible plants or varities
of these crops may remain free from infection or symptoms and thus appear
resistant.
Types:
• Disease escape: occurs whenever genetically susceptible plants do not
become infected because the three factors necessary for disease (susceptiblr
host, virulent pathogen and favourable environment) do not coincide and
interact at the proper time or for sufficient duration.
• Disease Tolerance: Tolerance to disease is the ability of plants to produce a
good crop even when they are infected with a pathogen.
 Tolerance results from specific, heritable characteristics of the host plants that
allow the pathogen to develop and multiply in the host while host, eiher by
lacking receptor sites for or by inactivating or compensating for the irritant
excretions of the pathogen, still manages to produce a good crop.
Boom and Bust Cycle
● A cycle where varieties possessing effective resistance (due to a single major
gene) are grown on an expanding acreage (boom) until matching virulence
evolves and spreads within the pathogen population (bust).
04
Thanks for your Attentions.....

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Hypersensitive Resoponse in plants and defence

  • 1. Hypersensitive Response in plants Dr. Joginder Pal Rao Asstt. Prof., Plant Pathology CSKHPKV Palampur
  • 4. Hypersensitive Response- a mechanism used by plants, to prevent spread of infection by microbial pathogens
  • 5. Definition: The plant hypersensitive response (HR) is a rapid localized cell death that occurs at the point of pathogen penetration and is associated with disease resistance. or • is a localized induced cell defense in the host plant at the sites of infection by the pathogen. • The hypersensitie response occurs only in specific host- pathogen combinations in which host and the pathogen are incombatible i.e. pathogen fails to infect the host  E.C.Stakman, 1915 was the first to use the term ‘hypersensitive’ in plant pathology
  • 10. • The hypersensitive response is the culmination of the plant defense responses initiated by: – the recognition by the plant of specific pathogen-produced signal molecules, known as elicitors. Recognition of the elicitors by the host plant activates a cascade of biochemical reactions in the attacked and surrounding plant cells and – leads to new or altered cell functions and to new or greatly activated defense-related compounds • The most common new cell functions and compounds include: – a rapid burst of reactive oxygen species, leading to a dramatic increase of oxidative reactions; – increased ion movement, especially of K+ and H+ through the cell membrane; – disruption of membranes and loss of cellular compartmentalization – production of antimicrobial substances such as phenolics (phytoalexins); and formation of antimicrobial so-called pathogenesis- related proteins such as chitinases.
  • 11. • The HR is characterized by the rapid death of cells in the local region surrounding an infection. The HR serves to restrict the growth and spread of pathogens to other parts of the plant. • The HR is analogous to the innate immune system found in animals, and commonly precedes a slower systemic (whole plant) response, which ultimately leads to systemic acquired resistance (SAR). • Result in sudden death of the host cells in the vicinity of the pathogen – Highest degree of resistance • Both structural & biochemical in nature • Common in obligate pathogens like fungi, viruses and nematodes, also found in other fungal & bacterial infection • Due to HR – The necrotic tissues isolate the obligate pathogen from living cells. – Devoid the pathogen of nutrition, thus starved and die.
  • 12. • The HR is triggered by the plant when it recognizes a pathogen. The identification of a pathogen typically occurs when virulence genes, secreted by a pathogen, bind to, or indirectly interact with the product of a plant resistance (R) gene. Plant R genes are highly polymorphic, and many plants produce several different types of R gene products, enabling them to recognize virulence products produced by many different pathogens. • In phase one of the HR, the activation of R genes triggers an ion flux, involving an efflux of hydroxide and potassium outside the cells, and an influx of calcium and hydrogen ions into the cell. • In phase two, the cells involved in the HR generate an oxidative burst by producing reactive oxygen species (ROS), superoxide anions, hydrogen peroxide, hydroxyl radicals and nitrous oxide. These compounds affect cellular membrane function, in part by inducing lipid peroxidation and by causing lipid damage. • The alteration of ion components in the cell, and the breakdown of cellular components in the presence of ROS, results in the death of affected cells and the formation of local lesions. Reactive oxygen species also trigger the deposition of lignin and callose, as well as the production of hydroxyproline-rich glycoproteins. These compounds serve to reinforce the walls of cells surrounding the infection, creating a barrier and inhibiting the spread of the infection.
  • 13. Consequences of HR  Depolarization of the membrane  Electrolyte leakage  Loss of selective membrane permeability  Apposition of material to the cell wall  Increased cytoplasmic streaming  Translocation of nucleus to infection site  Callose deposition and papillae formation  Condensation of nucleoplasm and cytoplasm  Disintegration of cytoskeleton  Cleavage of nuclear DNA  cells surrounding the lesion synthesize antimicrobial compounds, including phenolics, phytoalexins, and pathogenesis related (PR) proteins, including β-glucanases and chitinases
  • 14. 1. Non-host Resistance • When a plant resist the attack of pathogenic organism which is otherwise not the host of that pathogen is termed as non host resistance – e.g. potato late blight pathogen do not infect apple or wheat plant and similarly apple pathogen like V. inaequalis do not attack potato • Similarly, the fungus that causes powdery mildew on wheat (Blumeria (Erysiphe) graminis f. sp. tritici) does not infect barley and vice versa, the fungus that causes powdery mildew on barley (B. graminis f. sp. hordei) does not infect wheat, and so on.
  • 15. 2. True resistance • Disease resistance that is controlled genetically by the presence of one, a few or many genes for resistance in the plant is known as true resistance Types: • Horizontal resistance • Vertical resistance
  • 16. Horizontal resistance: • Also referred as partial, race non-specific quantitative, Durable, Field, Minor gene, polgenic or multigene resistance Vertical resistance: • Also known as strong, R-gene resistance, Major gene resistance, Race specific, Monogenic or oligogenic resistance
  • 17. Cytoplasmic resistance • In several plant diseases, resistance is controlled by genetic material contained/present in the cytoplasm of the cell. Such resistance is sometimes referred to as cytoplasmic resistance. • The two best examples of cytoplasmic resistance occur in the Southern corn leaf blight caused by Bipolaris (Helminthosporium) maydis and the Yellow leaf blight caused by Phyllosticta
  • 18. 3. Apparent Resistance • Under certain conditions or circumstances, some susceptible plants or varities of these crops may remain free from infection or symptoms and thus appear resistant. Types: • Disease escape: occurs whenever genetically susceptible plants do not become infected because the three factors necessary for disease (susceptiblr host, virulent pathogen and favourable environment) do not coincide and interact at the proper time or for sufficient duration. • Disease Tolerance: Tolerance to disease is the ability of plants to produce a good crop even when they are infected with a pathogen.  Tolerance results from specific, heritable characteristics of the host plants that allow the pathogen to develop and multiply in the host while host, eiher by lacking receptor sites for or by inactivating or compensating for the irritant excretions of the pathogen, still manages to produce a good crop.
  • 19. Boom and Bust Cycle ● A cycle where varieties possessing effective resistance (due to a single major gene) are grown on an expanding acreage (boom) until matching virulence evolves and spreads within the pathogen population (bust). 04
  • 20. Thanks for your Attentions.....