2. C O N T E N T S
1.Introduction
2.Biotic stress
3.Hypersensitive response
4.Secondary Acquired Resistance
5.Reference
6.Conclusion
3. INTRODUCTION
Biotic stress is the stress that occurs as a result
of damage done to an organism by an other
living organism.Such as
Bacteria,Viruses,Fungi, Parasites, Beneficial
and harmful insects, Weeds and Cultivated
or native plants.
4. It is different from abiotic stress, which is the
negative impact of non-living factors on the
organism such as Temperature,Sunlight, Wind,
Salinity,Flooding and Drought.
The damage caused by these living and non-living
agents can appear very similar.Even with close
observation accurate diagnosis can be difficult.
For example: Browning of leaves on an oak tree
caused by drought stress may appear similar to
leaf browning caused by oak wilt, a serious
vascular disease caused by a fungus.
5. The herbivore insects and disease caused
by fungi, bacteria and nematodes that are
ever present in the environment represent
potential biotic stresses in plants.
Although, plants do not have an immune
system as compared to animals, but the
plants have developed intricate defense
strategies including production of
secondary metabolites to ward off insects
6. The parts of diverse mechanisms adopted by
plants to resist infection are;
1. Hypersensitive response (HR)
2. Secondary acquired resistance (SAR)
7. 1.HYPERSENSITIVE RESPONSE
The Hypersensitive response is a mechanism used
by plants, to prevent the spread of infection by
microbial pathogens.
The Hypersensitive response serves to restrict the
growth and spread of pathogen to other parts of
the Plant.
8. On being attacked by insects or a pathogenic
microorganisms, typically a plant responds with,
1. Formation of pathogenesis-related proteins
2. Biosynthesis of phytoalexins
3. Changes in composition and physical
properties of cell walls
4. Process of programmed cell death
All these responses are collectively known as
Hypersensitive response or reaction (HR).
9. 1. FORMATION OF PATHOGENESIS-RELATED
PROTEINS
These are the products of defense-related
genes that are activated by microbial infection
and include hydrolytic enzymes such as,
A. Proteinase inhibitors which inhibit
activities of proteolytic enzymes secreted
by the pathogen.
B. Lytic enzymes such as glucanases,
chitinases and other hydrolases that
attack and degrade the cell walls of the
10. 2. BIOSYNTHESIS OF
PHYTOALEXINS
The microbial infection also activates genes that encode
enzymes for the synthesis of Phytoalexins.
Phytoalexins are a Chemical diverse group of secondary
metabolites (chiefly isoflavonoids and sesquiterpenes )
with strong antimicrobial activity.
The isoflavonoids medicarpin from Alfalfa and
Glyceolin from Soyabean, and Sesquiterpenes such as
rishitin from tomato and potato, and capsidol from
tobacco and pepper are well known examples of
11. 3. CHANGES IN COMPOSITION AND
PHYSICAL PROPERTIES OF HOST CELL
WALLS
In response to pathogen invasion, lignin, callose,
suberin and some hydroxy-proline rich
glycoproteins are synthesized and accumulated in
host cell walls to strengthen the latter and
physically blocking the spread of the invading
pathogen.
12. 4. PROGRAMMED CELL DEATH
The Hypersensitive response culminates in rapid
death of cells around the infection site depriving
pathogen of the nutrient supply and limiting it’s
spread in host plant and leaving necrotic
lesions at the site of invasion.
The rest of the plant however, remains
unaffected.
13. MECHANISM OF RECOGNITION OF THE POTENTIAL
PATHOGEN TO INITIATE DEFENSE RESPONSE IN
PLANTS
Not all plants are resistant to disease caused
by pathogens. Researchers have shown that
resistance of microbial pathogens has an
underlying genetic basis. The pathogens
carry avr genes (avirulence genes) while the
host plants carry corresponding resistance
genes called R genes. Diseases occurs when
the pathogen lacks avr genes or the host plant
does not carry dominant R genes.
14. 2. SECONDARY ACQUIRED RESISTANCE
(SAR)
The Hypersensitive response is limited to near vicinity
of the initial site of infection by pathogen. But, often
the entire host plants develops increased resistance
against pathogens over a period of time ranging from
few hours to several days following initial infection at
one site of the plant.
This phenomenon wherein “a single encounter with
the pathogen increases resistance to entire plant to
future attacks by pathogens” is called as secondary
15. SAR appears to result from increased levels of some
secondary metabolites and other defense
compounds such as chitinases and other hydrolytic
enzymes.
However,the mechanism of SAR is not clearly
understood. One component of the signaling
pathway is likely to be Salicylic acid (SA) that is
benzoic acid derivative and a secondary metabolite.
It has been shown in variety of plants that the
infection by pathogen results in increased levels of
SA in the zone of infection that establishes SAR in
17. According to Van Bel and Gaupels (2004), the
transmission of SAR signal from infection site to
other parts of the plant is very rapid and possibly
occurs through vascular tissue.
Phloem is now considered to be the pathway of
SAR signal.
Salicylic acid is not the mobile SAR signal.
Maldonado et.al., in 2002 have shown that in
Arabidopsis, mutations in DIR1 gene (Defective in
Induced Resistance 1 gene) inhibit SAR response.
18. been suggested that the long distance SAR
signal might be a substance derived from a
Apart from Phloem-mobile signals, the plant
may develop SAR through air-borne signals.
19. Salicylic acid may be converted into it’s methyl
ester, methyl Salicylate that is a moderately
volatile substance.
Methyl Salicylate may function as volatile air-
borne SAR-inducing signal that is transmitted
distant non-infected parts of the plant and even
to non-infected neighbouring plants making
them resistant to pathogen attack.
20. CONCLUSION
Recent researchers have shown that the Hypersensitive
response is preceded by accumulation of nitric oxide
and active Oxygen species.
The production of active oxygen species appears to be
prerequisite for activation of Hypersensitive response.
Induction of PCD is prevented in absence of any of these
two signals.