barriers that pathogens should cross to infest plants

2. Structural defense
in plants against
pathogens

3. Defense Mechanism in Plants
Constitutive or Induced
 Structural ( Morphological) defense
 Biochemical defense
Both the defenses are affected by:
 Age of the plant
 Type of organ infected
 Nutritional status of the host
 Environmental conditions

4. The defense may be
 Non-host Resistance
 Host Resistance

5. 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.
 Eg: potato late blight pathogen do not infect
apple or wheat plant.

6. Host defenses
 When a plant resist the attack of pathogenic
organism which is the host of that pathogen is
termed as host resistance or host defense.
 Among the structural host defenses, it may be
 Pre- existing structural defenses
 Post existing structural defenses

7. Pre existing/ pre- infectional
structural barriers
 Surface barrier
Presence of
 Wax layers
 Hairs
 Lignin
 Thickness of cuticle
 Spines
 Sub surface barriers
 Epidermal cells
 Stomata
 Lenticels
 Hydathodes

9. Wax layer
•Highly repellent.
•Fatty acids are one
of hydrophobic
compound.

10.  Resistance against fungi and bacteria.
 Obstruct the path of infection tube.
 Acts as a carrier of applied fungicides.

11. Hairs
•Thick mat of hairs on plant surface reduce
infection.
•Induce water repelling effect.

12. 1- Root hairs
2- Hairs on
stem
3- Hairs on
leaves

13. Lignin
Prevents infection due to the toughness.

14. Cuticle

15. Cutin
 Plants’ cuticles
often vary with the
climate in which
they live.
Cactus cuticle
Cactus cuticle

16.  Cuticle defend the underlying tissues by,
 Water repellent capacity
 Negative electric charge
 Toxicity to some pathogen
 Mechanical obstructions.

17. Imparts resistance against direct penetrating
pathogens.
 e.g.
Puccinea graminis tritici.

18. Epidermis
 May directly impede entrance of the pathogens.
 The degree of impediment depends on,
i)thickness of the outer epidermis and
ii)toughness – due to variation in relative
lignifications and salicic acid deposition.

19. Eg:
 Amount of salicic acid in leaves against blast in rice .

20.  P. graminis tritici shows varied degree of
susceptibility i.e, young plants are more susceptible.

21. Formation of Appressorium and penetrating
Hyphae of Puccinia grisea on different cells of
Rice
EPIDERMAL
CELLS
PERCENT FORMATION
APPRESSORIA INFECTION
HYPHAE
Motor cells 53.0 63.7
Long cells 16.2 7.9
Short cells 12.8 6.1
Hairs 1.7 -
Stomata 6.0 -

22. Stomata
Mainly restricts bacteria
which enters through
passive mode.
Structure, number and
location decides extent of
resistance.
Eg:
 Mandarins resistant to
Xanthomonas axanopodis
has stomata surronded by
raised broad -lip like
structure.

23.  Location and shape of stomata, opening & closing
mechanisms -resistant wheat varieties for Rusts.

24.  Size of stomata - Resistant citrus vars have small
stomata against X. campestris

25. Lenticels
 Plant parasitic bacteria and fungus enters through
lenticels
 The shape and internal structure plays a role .
 Suberin layer beneath it restrict the entry.

26. Suberin
 often within roots.
 can protect against pathogens and other damage.
 older parts of roots more suberized
 endodermis has suberin side walls, water
must pass through plasma membrane to get to stele

27. Suberin can form transport barriers
between the soil and the roots

28. Hydathodes and Nectarthodes
 Entry point for bacterial pathogens.
 Sugary nectar serves as barrier to pathogens due
to high osmotic pressure.

29. Stem spines Colletia paradoxa Leaf spines- Opuntia invicta
Shoot spines- Dovyalis caffra
Otherwise known as kei apple
Drought tolerant

30. Post infectional defense
structures
 Histological defense
 Tylose formation e.g. wilts
 Corky layers e.g. in potato- R. solani
 Cellular defense
 Cytoplasmic defense
 Hypersensitive response.

31. Tylose formation
 Tyloses are the
overgrowths
of living cells that
protrude via pits into
xylem vessels
blocking the vascular
system.

32.  If they form
abundantly and
quickly, they can
stop the spread of
vascular wilt
pathogens.
 Their formation is
triggered by a “stress
condition”.

33. Cork layer
 Limits the size of lesion formation.

34. Eg:
 Formation of cork layer on potato tubers

35. Abscission layer
 Formed between the infected and healthy cells or
tissues of plants.

36. The formation of abscission layers can,
 Limit the size of lesions.
 Delimits the extent of damage that can be caused by
a single infection.
 Prevents the further spread of pathogen.

37.  Schematic formation of
abscission layer around the
diseased spots.
 Eg:
Xanthomonas pruni-shot
hole of Prunus leaf

38. 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.

39. Hypersensitive response
o Highest degree of resistance.
o Result in sudden death of the host cells in the vicinity
of the pathogen.
o Both structural & biochemical in nature.
o Common in obligate pathogens like fungi, viruses
and nematodes, also found in other fungal &
bacterial infection.
o Due to HR
– The necrotic tissues isolate the obligate
pathogen from living cells.
– Devoid the pathogen of nutrition, thus starved
and die.