study material regarding HR, which included mechanisms and activities of HR in plants against plant pathogen

1. Hypersensitive reaction and mechanisms
 The term hypersensitivity is literally barrowed from human medicine terminology.
Literally, it means that an organism or group of organisms are sensitive to a
pathogenic agent
 However the hypersensitivity concept from in plant pathology differs essentially
from the same term of human medicine, thus no analogue conclusion can be drawn
from examples in plant pathology
 Synonyms – suprasensitivity, hypersuceptability, hyperergy
 The Cambridge Botanist, Ward was 1st to recognise significance of hypersensitivity as
a defence mechanism of plant against plant pathogens (parasites)
 He shows that the pathogen penetrates with its hyphae into resistant as well as
susceptible host and he also observed no difference between the behaviour of the
resistant and susceptible host plant until direct, physiological contact is established.
 Ward recognised both extremes ‘highest resistance’ and ‘highest tolerance’ are
connected and mode of reaction is influenced by environmental factors.
 Why a pathogen such as Puccinia dispersa discontinues its growth prematurely in the
hypersensitivity host he endeavoured to some body in the cell sap of the host plant
which inhibits or promotes the growth of the fungus. These efforts failed and he
emphasizes the experiments teach very little
 After 10 later the research phenomenon described by Ward further gained a
breakthrough impetus from Stakman. His discovery that Erikson’s ‘forma specials’ of
the cereal rust fungus consists of man physiological races gave further progression in
hypersensitivity research
 Hypersensitivity –
 The term hypersensitivity was introduced by E. C. Stakman in physiological
plant pathology.
 HR is a cell defence mechanism or type or programmed cell death, that can
be used by host plants which prevents the spread of disease caused by
pathogen
 Characterised by rapid death (autolysis) of cells around the infection area
 Due to autolysis it prevents the rapid spread of disease to other parts of the
plants
 Mostly hypersensitive response associated with the death of a small number
of cells at and around the site of infection
 During HR, the dying plant cells strengthen their cell walls and accumulate
certain toxic compounds like phenols and phytoalexins
(Ward observed some changes that the tissue turned to brown and die
destructing activity of infecting cells and kills too rapidly, in the same time it
also ceases pathogen growth. Thereby, infection limited to localised necrotic
tissue and plant escapes the diseases)
 The HR occurs only in specific host-pathogen combination in which the host
and pathogen are incompatible.
 Its occur only in Vertical resistance

2.  Mechanism –
 The plant ‘hypersensitive response’ (HR), a defense mechanism, involves
interaction between products of an ‘avr’ gene of the pathogen and a
matching ‘R’ gene of the plant
 Plant HR is the result of an ‘incompatible reaction’, in which the ‘R’ gene of
the non-host plant corresponds to the ‘avr’ gene of the pathogen, where as
in a ‘compatible reaction’ the ‘R’ gene of the host plant does not match with
the ‘avr’ gene of the pathogen resulting in the spread of pathogen
throughout the plant and disease occurs
 This compatible reaction between ‘R’ gene and elicitor activates the
biochemical reaction and defence related compounds 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, hydroge
peroxide, hydroxyl radicals and nitrous oxide. These compounds
affect cellular membrane function, in part by inducing lipid peroxidation and
by causing lipid damage
 This results in the death of affected cells and formation of local lesions
 This actions will increases the production of salysilic acid (SAR), jasmonic acid
and ethylene (ISR)
 SAR triggered by bio-trophic pathogen
 ISR triggered by necrotrophic pathogen
 At end of the HR
 Depolarization of the membrane
 Electrolyte leakage
 Loss of selective membrane permeability
 Apposition of material to the cell wall
 Increased cytoplasmic streaming
 Translocation of the nucleus to infection site
 Callose deposition and papillae formation
 Condensation of Nucleoplasm and cytoplasm
 Disintegration of Cytoskeleton
 Cleavage of nuclear DNA
 In 1946, E. Gaümann proposed that in many host–pathogen combinations
plants remain resistant through hypersensitivity; i.e., the attacked cells are so
sensitive to the pathogen that they and some adjacent cells die immediately
and in that way they isolate or cause the death of the pathogen
 In the early 1960s, it was proposed that, in some cases, disease resistance is
brought about by phytoalexins, i.e., antimicrobial plant substances that either
are absent or are present at non detectable levels in healthy plants, but
accumulate to high levels in response to attack by a pathogen

3.  In bacteria T3SS (type 3 secretion system) plays a major role in hypersensitivity
 Although many explanations has been put forward in the past, such as virulence o the
pathogen, nutritional status of the host, and the toxins and enzymes of the pathogen.
 It has been reported that HR is associated with loss of turgor as reflected in the loss of
membrane permeability