2. The term was barrowed from human medicine
terminology
(organism or group of organisms, which are sensitive to a
pathogen agent)
Synonyms – suprasensitivity,
hypersuceptability,
hyperergy
3. Coming to plant pathology …………….
Ward (The Cambridge Botanist) 1st to recognise
significance of hypersensitivity as a defence mechanism
of plant against plant pathogens (parasites)
He observed no difference between the behaviour of the
resistant and susceptible host plant until direct,
physiological contact is established.
4. Ward recognised both extremes ‘highest resistance’ and
‘highest tolerance’ are connected and mode of reaction
is influenced by environmental factors.
But …..
why a pathogen such as Puccinia dispersa discontinues
its growth prematurely in the hypertensive host …
5. After 10 yrs ward gained breakthrough form
Stakman… that he discovered Eriksons phenomenon
f.sp. of rust fungus contains many physiological races
6. Hypersensitive response (HR) Stakman,
1915
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
• The term hypersensitivity was introduced in plant pathology by E .C.
Stakman, 1915
• Due to variability among plant pathogen, stakman called the
pathogen as “Shifty enemies”
7.
8. 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
9. After infection ……………
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
(Ward. 1902)
10.
11. The HR is the culmination of the plant defence
responses initiated by the recognition of specific
pathogen signal molecules, known as elicitors by
plant.
12. The HR occur only in specific host-pathogen
combination in which the host and pathogen are
incompatible.
Its occur only in Vertical resistance.
13. Mechanism
• Defense mechanism, involves interaction between
products of an ‘avr’gene of the pathogen and a matching
‘R’ gene of the plant
(Dodds et al., 2006).
This compatible reaction between ‘R’ gene and elicitor
activates the biochemical reaction and defence related
compounds
14.
15. 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
16. 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
18. Some biochemical reactions and
physiological aspects of hypersensitivity
Respiration rate, oxidise levels, peroxidase level
and mitochondrial number (Kiraly, 1980)
Phenolic and flavonoid compounds are increased
(Loebenstein, 1972)
19.
20. 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
21. 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.
22. 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
23. References
George N Agrios, 2005. Plant Pathology 5th Edition pp221-
237
Horsfall, J.G. ed., 2012. Plant Pathology V1: The Diseased
Plant. Elsevier.
Kiraly, Z. 1980. Defenses triggered by the invader:
hypersensitivity, pp. 201-225. In J. Horsfall & E. B. Cowling
[eds.], Plant diseases, vol. V. Academic, New York.
Loebenstein, G. 1972. Localization and induced resistance
in virus-infected plants. Annu. Rev. Phytopathol. 10: 177-
206.
Balint‐Kurti, P., 2019. The plant hypersensitive response:
concepts, control and consequences. Molecular plant
pathology, 20(8), pp.1163-1178.