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MOHD TARIQ
(Research scholar)
Section of Plant Pathology and Nematology
Department of Botany A.M.U, Aligarh
RESISTANCE
The ability of an organism to exclude or overcome completely
or in some degree, the effect of a pathogen, or other damaging
factor.
Non-Host Resistance
Plants are resistant to certain pathogen either because they
belong to taxonomic groups that are outside the host range of
these pathogens.
Gene For Resistance
They posses gene for resistance (R gene) directed against the
gene for virulence of the pathogen.
INTRODUCTIO
N
TRUE RESISTANCE
Disease resistance that is genetically controlled by the presence
of one, a few or many genes for resistance in the plants is known
as True resistance.
In true resistance the host and the pathogen are more or less
incompatible with one another either because of the lack of the
chemical recognition between the host and the pathogen.
TYPES
1. Horizontal resistance
2. Vertical resistance
1. Horizontal resistance
Such resistance is also called non-specific, general, quantitative,
adult plants, field or durable resistance but it is most commonly
known as horizontal resistance.
Horizontal resistance is controlled by many type of genes so it is
also called Polygenic resistance.
2. Vertical resistance
Such resistance is also called strong, major, specific, qualitative
or differential resistance but it is most commonly known as
vertical resistance.
Vertical resistance is always controlled by one gene so it is also
called monogenic resistance.
APPARENT RESISTANCE
In any area, and almost every year, limited or widespread plant
disease epidemics occur on various crop plants.
The apparent resistance to disease of plants known to be
susceptible is generally the result of disease escape or tolerance to
disease.
DISEASE ESCAPE
Disease escape occurs whenever genetically susceptible plants do
not become infected because the three factor necessary for disease
do not coincide.
1.Susceptible host
2.Virulent pathogen
3.Favourable environment
PREEXISTING STRUCTURAL AND CHEMICAL DEFENSES
Preexisting structural defense
Wax
Thick cuticle
Thickness and toughness of the outer wall of epidermal cells
Stomata
Sclerenchyma cells
Lenticel
Preexisting chemical defense
1. Inhibitors
Released by plant in it’s environment
Present in plant cells before infection
2. Phenolics
Tannins
Glucanases
Dienes
Chitinase
INDUCED STRUCTURAL AND CHEMICAL DEFENSES
Induced structural defense
Cytoplasmic defense reaction
Cell wall defense structure
Histological defense structure
Formation of cork layer
Formation of abscission layer
Formation of tyloses
Deposition of gums
Induced chemical defense
Hypersensitivity response (HR)
Production of Antimicrobial substances
Pathogenesis- Related Protein (PR Protein)
Phytoalexins
Systemic acquired Resistance
PREEXISTING STRUCTURAL DEFENSE
Some structural defense are present in the plant even before the
pathogen comes in contact with the plant.
1. WAXES
 Waxes is a general term used to the mixture of long-chain
apolar lipids forming a protective coating (cutin in the
cuticle) on plant leaves and fruits
 Synthesized by epidermal cells
 Extremely hydrophobic
 Waxes form outer coating of the cuticle
 Often crystallizes in pattern of rods, tubes or plates
2. THICK CUTICLE
Plant cuticle are protective, hydrophobic, waxy covering
produced by the epidermal cells of leaves, young shoots and all
other aerial plant organ.
Thickness of cuticle e.g. in resistant flax Melampsora lini,
Barberry-Puccinia graminis tritici
3.THICKNESS AND TOUGHNESS OF THE OUTER WALL
OF EPIDERMAL CELLS
The thickness and toughness of outer wall of epidermal cells are
apparently important factors in the resistance of some plants to
certain pathogen.
Thick, tough walls of epidermal cells make direct penetration by
fungal pathogens difficult or impossible.
 For example Barberry- Puccinia graminis tritici resistance is
attributed to the tough outer epidermal cells.
4.STOMATA
The minute pores in the epidermis of leaf through which
exchange of gases takes place.
Size of stomata (Resistant citrus vars. have small stomata-
Xanthomonas campestris)
Location and shape of stomata, opening and closing (resistant
wheat vars. – Rust).
5. SCLERENCHYMA CELLS
Composed of walls thickened with lignin
Have brittle cells helps in mechanical support to plants
These cells effectively blocks spread of fungal and bacterial
pathogen that cause angular leaf spot
For example some wheat varieties resistant to stem rust-stem
contain high sclerenchyma cells.
6. LENTICEL
Lenticels are airy cells in the bark of stem and roots
The shape and internal structure of lenticels can increase and
decrease the incidence of fruit disease
Lenticels of small size restrict entry of pathogen.
PREEXISTING CHEMICAL DEFENCE:
Although structural characteristics may provide a plant with
various degree of defence against attacking pathogens.
It is clear that the resistance of a plant against pathogen attack
depends not so much on its structural barriers as on the substances
produced in its cell before or after infection.
INHIBITORS RELEASED BY THE PLANT IN IT’S
ENVIRONMENT
Plants exude a variety of substances through the surface of their
aboveground parts as well as through the surface of their roots.
 Fungitoxic exudates- on the leaves of some plants, e.g. tomato and
sugarbeet inhibit the germination of Botrytis and Cercospora
Oil capric acid on elm seed toxic to Ceratocystis ulmi spores
Phenolics: red scale onion against smudge –Colletotrichum
circinans
Onion smudge
Susceptible
Resistant
INHIBITORS PRESENT IN PLANT CELLS BEFORE
INFECTION
It is becoming increasingly apparent that some plants are
resistant to disease caused by certain pathogen of an inhibitory
compound present in the cell before infection.
Stored in vacuoles, lysogenous glands, heart wood periderm
of plants
Phenolics – onion (catechol and protocatechuic acid )
Saponins (tomatin in tomato, avenacin in oats ) most of these
compounds inhibits hydrolytic enzymes produced by pathogen
e.g. pectolytic enzymes etc.
Tannins, and some fatty acid-like compound such as dienes,
which are present in high concentrations in cells of young
fruits, leaves or seeds.
Some plants also contains hydrolytic enzymes e.g.
glucanases, chitinases etc.
INDUCED STRUCTURAL AND CHEMICAL DEFENSES
INDUCED STRUCTURAL DEFENSE
 Cytoplasmic Defense Reaction
Some of the defense structures formed involve the cytoplasm of the cells
under attack, and the process is called cytoplasmic defense reaction.
Cell Wall Defense Structure
It involve morphological changes in the cell wall or change derived from
the cell wall of the cell being invaded by the pathogen.
Three main types of such structures have been observed in plant diseases.
The outer layer of the cell wall of parenchyma cells coming in contact with
incompatible bacteria swells and produced an amorphous, fibrillar material
that surrounds and traps the bacteria and prevents them from multiplying.
Cell walls thicken in response to several pathogens by producing what
appears to be a cellulosic material.
Callose papillae are deposited on the inner side of cell walls in response to
invasion by fungal pathogen.
 Histological Defense Structures
 Formation Of Cork And Abscission Layer
The formation of cork or abscission layers can limit the size of lesions, and
consequently the extent of damage that can be caused by a single
infection.
e.g. Cork layer Rhizoctonia solani canker in potato
Abscission layer Xanthomonas pruni shot hole
Provide protection by -
Inhibiting the further
spread of pathogen
Block the spread of
toxic substances of the
pathogen
stop the flow of
nutrients to infection
point
Tyloses
Tyloses are overgrowth of living cells that protrude via pits into
xylem vessels blocking the vascular system.
If they form abundantly and quickly, they can stop the spread of
vascular wilt pathogens.
Their formation is triggered by a “stress condition”.
DEPOSITION OF GUM
 Various types of gums are produced by many plants
around lesions after infection by pathogen or injury.
 Gums secretion is most common in stone fruit trees but
occurs in most plants.
 Generally these gums are exudated by plant due to the
stressed condition.
 The production gum by these trees by the process
called as gummosis.
INDUCED CHEMICAL DEFENSE
HYPERSENSITIVE RESPONSE (HR)
The hypersensitive response is localized death of host cells at
the site of infection.
It is the result of a specific recognition of a pathogen attack by
the host.
The HR is considered to be a type of programmed cell death.
 The hypersensitive response is the culumination of the plant
defense response 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, leads to new or altered cell functions and to new or greatly
activated defense- defense related compounds.
 The most common new cell functions and compound include:
 A rapid burst of reactive oxygen species, leading to a dramatic
increase of oxidative reaction.
 Increased ion movement, especially of K+ and H+ through the
cell membrane.
 PRODUCTION OF ANTIMICROBIAL SUBSTANCES
 PATHOGENESIS- RELATED PROTEINS (PR-
PROTEINS)
 Pathogenesis related proteins, called PR- proteins- A group of
plant coded proteins
 Are structurally diverse group toxic to invading pathogens.
 Produced under stress
 They are widely distributed in plants in trace amounts but are
produced in high concentration following pathogen attack or
stress.
 The PR proteins exist in plant cells intracellularly (acidic in
Apoplast & basic form in vacuoles) and also in the intercellular
spaces.
 Varying types of PR- proteins have been isolated from several
crop plants.
Groups of PR- proteins
 The better known PR protein are:
 PR- 1 proteins, B-1,3-glucanases, chitinases, lysozymes
 PR 4 proteins, thaumatinelike proteins, osmotinlike
proteins, cysteine-rich proteins, glycine-rich proteins,
proteinase inhibitors, proteinases and peroxidases. There
are often numerous isoforms of each PR- protein in
various host plants.
PHYTOALEXINS
Concept given by Borger & Muller in Potato- late blight
interactions
Defined as antibiotics produced in plant- pathogen interaction or
as a response to injury or physiological stimuli
Paxton (1981) defined phytoalexins as low molecular weight
antimicrobial compounds which are synthesized by and
accumulates in plant cells after microbial infection.
Involves the role of elicitors in their production
Not produced during bio trophic infection.
E.g. Leguminosae, Solanaceae, Malvaceae, Graminae,
Compositae, Umbelliferae and Chenopodiaceae.
 SYSTEMIC ACQUIRED RESISTANCE (SAR)
 SAR confers broad-based resistance to different pathogens.
For example, primary inoculation with a fungal leaf spot
pathogen reduces susceptibility of the host plant to other fungi
as well as to bacterial and viral pathogens.
 Salicylic acid (chemical related to aspirin) is part of signaling
pathway involved in transmission of the defense response
throughout the plant to produce SAR. This has lead to the
development of synthetic chemicals that mimic the role of
salicylic acid.
Induction of Systemic Acquired Resistance
Production of H2O2 (plus antioxidants)
Hydrogen peroxide has been associated
secondary induction of SAR and direct toxic
activity to invading pathogens
Thickening of plant cell wall Production of
phenolic (lignin, tannic acid) that strengthen
walls and inhibit pathogen enzymes
Accumulation of pathogenesis related
proteins “PR-proteins” chitinases, ß-1,3
Glucanases.
These enzymes accumulate in vacuole of
plant cell. Upon attack, they directly degrade
fungal cell walls. Indirectly, their action
results in the release of fungal wall
components that elicit additional defense
reactions
Sprayed
inducer
(activator) that
mimics
salicyclic acid
CONCLUSION
 Under favourable condition the infection(susceptibility) or non-
infection (resistance) in each host-pathogen combination is
predetermined by the genetic material of the host and of the
pathogen.
 In some diseases however, particularly those caused by fungi,
such as potato late blight, apple scab, powdery mildews, tomato
leaf mould, and the cereal smuts and rust, and also in several
viral and bacterial disease of plants, considerable information
regarding the genetics of host-pathogen interaction is available.
REFERENCES:
PLANT PATHOLOGY
- GEORGE N. AGRIOS
Defence mechanism in plants: Preformed substances and structures.

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Defence mechanism in plants: Preformed substances and structures.

  • 1. MOHD TARIQ (Research scholar) Section of Plant Pathology and Nematology Department of Botany A.M.U, Aligarh
  • 2. RESISTANCE The ability of an organism to exclude or overcome completely or in some degree, the effect of a pathogen, or other damaging factor. Non-Host Resistance Plants are resistant to certain pathogen either because they belong to taxonomic groups that are outside the host range of these pathogens. Gene For Resistance They posses gene for resistance (R gene) directed against the gene for virulence of the pathogen. INTRODUCTIO N
  • 3. TRUE RESISTANCE Disease resistance that is genetically controlled by the presence of one, a few or many genes for resistance in the plants is known as True resistance. In true resistance the host and the pathogen are more or less incompatible with one another either because of the lack of the chemical recognition between the host and the pathogen. TYPES 1. Horizontal resistance 2. Vertical resistance
  • 4. 1. Horizontal resistance Such resistance is also called non-specific, general, quantitative, adult plants, field or durable resistance but it is most commonly known as horizontal resistance. Horizontal resistance is controlled by many type of genes so it is also called Polygenic resistance. 2. Vertical resistance Such resistance is also called strong, major, specific, qualitative or differential resistance but it is most commonly known as vertical resistance. Vertical resistance is always controlled by one gene so it is also called monogenic resistance.
  • 5. APPARENT RESISTANCE In any area, and almost every year, limited or widespread plant disease epidemics occur on various crop plants. The apparent resistance to disease of plants known to be susceptible is generally the result of disease escape or tolerance to disease. DISEASE ESCAPE Disease escape occurs whenever genetically susceptible plants do not become infected because the three factor necessary for disease do not coincide. 1.Susceptible host 2.Virulent pathogen 3.Favourable environment
  • 6. PREEXISTING STRUCTURAL AND CHEMICAL DEFENSES Preexisting structural defense Wax Thick cuticle Thickness and toughness of the outer wall of epidermal cells Stomata Sclerenchyma cells Lenticel Preexisting chemical defense 1. Inhibitors Released by plant in it’s environment Present in plant cells before infection 2. Phenolics Tannins Glucanases Dienes Chitinase
  • 7. INDUCED STRUCTURAL AND CHEMICAL DEFENSES Induced structural defense Cytoplasmic defense reaction Cell wall defense structure Histological defense structure Formation of cork layer Formation of abscission layer Formation of tyloses Deposition of gums Induced chemical defense Hypersensitivity response (HR) Production of Antimicrobial substances Pathogenesis- Related Protein (PR Protein) Phytoalexins Systemic acquired Resistance
  • 8. PREEXISTING STRUCTURAL DEFENSE Some structural defense are present in the plant even before the pathogen comes in contact with the plant. 1. WAXES  Waxes is a general term used to the mixture of long-chain apolar lipids forming a protective coating (cutin in the cuticle) on plant leaves and fruits  Synthesized by epidermal cells  Extremely hydrophobic  Waxes form outer coating of the cuticle  Often crystallizes in pattern of rods, tubes or plates
  • 9. 2. THICK CUTICLE Plant cuticle are protective, hydrophobic, waxy covering produced by the epidermal cells of leaves, young shoots and all other aerial plant organ. Thickness of cuticle e.g. in resistant flax Melampsora lini, Barberry-Puccinia graminis tritici
  • 10. 3.THICKNESS AND TOUGHNESS OF THE OUTER WALL OF EPIDERMAL CELLS The thickness and toughness of outer wall of epidermal cells are apparently important factors in the resistance of some plants to certain pathogen. Thick, tough walls of epidermal cells make direct penetration by fungal pathogens difficult or impossible.  For example Barberry- Puccinia graminis tritici resistance is attributed to the tough outer epidermal cells. 4.STOMATA The minute pores in the epidermis of leaf through which exchange of gases takes place. Size of stomata (Resistant citrus vars. have small stomata- Xanthomonas campestris) Location and shape of stomata, opening and closing (resistant wheat vars. – Rust).
  • 11. 5. SCLERENCHYMA CELLS Composed of walls thickened with lignin Have brittle cells helps in mechanical support to plants These cells effectively blocks spread of fungal and bacterial pathogen that cause angular leaf spot For example some wheat varieties resistant to stem rust-stem contain high sclerenchyma cells. 6. LENTICEL Lenticels are airy cells in the bark of stem and roots The shape and internal structure of lenticels can increase and decrease the incidence of fruit disease Lenticels of small size restrict entry of pathogen.
  • 12. PREEXISTING CHEMICAL DEFENCE: Although structural characteristics may provide a plant with various degree of defence against attacking pathogens. It is clear that the resistance of a plant against pathogen attack depends not so much on its structural barriers as on the substances produced in its cell before or after infection. INHIBITORS RELEASED BY THE PLANT IN IT’S ENVIRONMENT Plants exude a variety of substances through the surface of their aboveground parts as well as through the surface of their roots.  Fungitoxic exudates- on the leaves of some plants, e.g. tomato and sugarbeet inhibit the germination of Botrytis and Cercospora Oil capric acid on elm seed toxic to Ceratocystis ulmi spores Phenolics: red scale onion against smudge –Colletotrichum circinans
  • 14. INHIBITORS PRESENT IN PLANT CELLS BEFORE INFECTION It is becoming increasingly apparent that some plants are resistant to disease caused by certain pathogen of an inhibitory compound present in the cell before infection. Stored in vacuoles, lysogenous glands, heart wood periderm of plants Phenolics – onion (catechol and protocatechuic acid ) Saponins (tomatin in tomato, avenacin in oats ) most of these compounds inhibits hydrolytic enzymes produced by pathogen e.g. pectolytic enzymes etc. Tannins, and some fatty acid-like compound such as dienes, which are present in high concentrations in cells of young fruits, leaves or seeds. Some plants also contains hydrolytic enzymes e.g. glucanases, chitinases etc.
  • 15. INDUCED STRUCTURAL AND CHEMICAL DEFENSES INDUCED STRUCTURAL DEFENSE  Cytoplasmic Defense Reaction Some of the defense structures formed involve the cytoplasm of the cells under attack, and the process is called cytoplasmic defense reaction. Cell Wall Defense Structure It involve morphological changes in the cell wall or change derived from the cell wall of the cell being invaded by the pathogen. Three main types of such structures have been observed in plant diseases. The outer layer of the cell wall of parenchyma cells coming in contact with incompatible bacteria swells and produced an amorphous, fibrillar material that surrounds and traps the bacteria and prevents them from multiplying. Cell walls thicken in response to several pathogens by producing what appears to be a cellulosic material. Callose papillae are deposited on the inner side of cell walls in response to invasion by fungal pathogen.
  • 16.  Histological Defense Structures  Formation Of Cork And Abscission Layer The formation of cork or abscission layers can limit the size of lesions, and consequently the extent of damage that can be caused by a single infection. e.g. Cork layer Rhizoctonia solani canker in potato Abscission layer Xanthomonas pruni shot hole Provide protection by - Inhibiting the further spread of pathogen Block the spread of toxic substances of the pathogen stop the flow of nutrients to infection point
  • 17. Tyloses Tyloses are overgrowth of living cells that protrude via pits into xylem vessels blocking the vascular system. If they form abundantly and quickly, they can stop the spread of vascular wilt pathogens. Their formation is triggered by a “stress condition”.
  • 18. DEPOSITION OF GUM  Various types of gums are produced by many plants around lesions after infection by pathogen or injury.  Gums secretion is most common in stone fruit trees but occurs in most plants.  Generally these gums are exudated by plant due to the stressed condition.  The production gum by these trees by the process called as gummosis.
  • 19. INDUCED CHEMICAL DEFENSE HYPERSENSITIVE RESPONSE (HR) The hypersensitive response is localized death of host cells at the site of infection. It is the result of a specific recognition of a pathogen attack by the host. The HR is considered to be a type of programmed cell death.
  • 20.  The hypersensitive response is the culumination of the plant defense response 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, leads to new or altered cell functions and to new or greatly activated defense- defense related compounds.  The most common new cell functions and compound include:  A rapid burst of reactive oxygen species, leading to a dramatic increase of oxidative reaction.  Increased ion movement, especially of K+ and H+ through the cell membrane.
  • 21.  PRODUCTION OF ANTIMICROBIAL SUBSTANCES  PATHOGENESIS- RELATED PROTEINS (PR- PROTEINS)  Pathogenesis related proteins, called PR- proteins- A group of plant coded proteins  Are structurally diverse group toxic to invading pathogens.  Produced under stress  They are widely distributed in plants in trace amounts but are produced in high concentration following pathogen attack or stress.  The PR proteins exist in plant cells intracellularly (acidic in Apoplast & basic form in vacuoles) and also in the intercellular spaces.  Varying types of PR- proteins have been isolated from several crop plants.
  • 22. Groups of PR- proteins  The better known PR protein are:  PR- 1 proteins, B-1,3-glucanases, chitinases, lysozymes  PR 4 proteins, thaumatinelike proteins, osmotinlike proteins, cysteine-rich proteins, glycine-rich proteins, proteinase inhibitors, proteinases and peroxidases. There are often numerous isoforms of each PR- protein in various host plants.
  • 23. PHYTOALEXINS Concept given by Borger & Muller in Potato- late blight interactions Defined as antibiotics produced in plant- pathogen interaction or as a response to injury or physiological stimuli Paxton (1981) defined phytoalexins as low molecular weight antimicrobial compounds which are synthesized by and accumulates in plant cells after microbial infection. Involves the role of elicitors in their production Not produced during bio trophic infection. E.g. Leguminosae, Solanaceae, Malvaceae, Graminae, Compositae, Umbelliferae and Chenopodiaceae.
  • 24.  SYSTEMIC ACQUIRED RESISTANCE (SAR)  SAR confers broad-based resistance to different pathogens. For example, primary inoculation with a fungal leaf spot pathogen reduces susceptibility of the host plant to other fungi as well as to bacterial and viral pathogens.  Salicylic acid (chemical related to aspirin) is part of signaling pathway involved in transmission of the defense response throughout the plant to produce SAR. This has lead to the development of synthetic chemicals that mimic the role of salicylic acid.
  • 25. Induction of Systemic Acquired Resistance Production of H2O2 (plus antioxidants) Hydrogen peroxide has been associated secondary induction of SAR and direct toxic activity to invading pathogens Thickening of plant cell wall Production of phenolic (lignin, tannic acid) that strengthen walls and inhibit pathogen enzymes Accumulation of pathogenesis related proteins “PR-proteins” chitinases, ß-1,3 Glucanases. These enzymes accumulate in vacuole of plant cell. Upon attack, they directly degrade fungal cell walls. Indirectly, their action results in the release of fungal wall components that elicit additional defense reactions Sprayed inducer (activator) that mimics salicyclic acid
  • 26. CONCLUSION  Under favourable condition the infection(susceptibility) or non- infection (resistance) in each host-pathogen combination is predetermined by the genetic material of the host and of the pathogen.  In some diseases however, particularly those caused by fungi, such as potato late blight, apple scab, powdery mildews, tomato leaf mould, and the cereal smuts and rust, and also in several viral and bacterial disease of plants, considerable information regarding the genetics of host-pathogen interaction is available.