The document discusses the complex interactions between plants and pathogens, detailing types of pathogens, their effects, and plant immune responses. It outlines models of recognition and defense mechanisms, including the gene-for-gene hypothesis and various interaction models such as the elicitor-receptor and guard hypotheses. The conclusion emphasizes the specificity and dynamism of plant-pathogen interactions, with defense signaling initiated by pathogen recognition.

1. sheikh Mansoor shafi
Division of Biochemistry
SKUAST-J

2. HOST-PATHOGEN INTERACTION
Disease is a disfunction of normal
physiological processes in plants
caused by microorganisms or an
abiotic factor.
• A pathogen that causes
diseases is termed virulent
• A pathogen that does not
cause diseases is termed
avirulent
Types of pathogen based on
effects:
• necrotrophy: plant cells are
killed
• biotrophy: plant cells remain
alive
• hemibiotrophy:plant cells
initially alive and killed later

3. Types of pathogen based on effects:
• Necrotrophy: plant cells are killed
• Biotrophy: plant cells remain alive
• Hemibiotrophy:plant cells initially alive and
killed later

5. Types of Pathogens
• Bacteria: Enter through wounds or stomata, live
between plant cells.
• Fungi: filamentous growth with specialized
structures for penetration, feeding in cells. Can
penetrate directly into plant and move
intercellularly or through cells.
• Viruses: Nucleic acid (+ RNA mostly) encapsulated
in a protein coat-Spread by plasmodesmata.

6. Classes of plant immune
responses
• Basal response: transcription of genes in
response to PAMP recognition.
• Hypersensitive response (HR); apoptosis of cells
at the site of infection
• Systemic acquired immunity: The entire plant
becomes resistant to infection
• Jasmonic acid/ethylene pathway: The entire
plant and neighboring plants develop resistance
to herbivores.
• Non-host immunity

7. INDUCED DEFENCE
Induced defence
Programmed cell death
(PCD)
Induced structural barriers
phytoalexins
Pathogenesis related
proteins (PR-proteins)
Post transcriptional gene
silencing (PTGS)
Heil, M., and R.M. Bostock. 2002

8. STEPS IN PLANT-PATHOGEN
INTERACTION
RECOGNITION-depends on generation of
elicitors by the pathogen (Diseases/Non Diseses)
 TRANSDUCTION: Signal transduction at the
cellular level refers to the movement of signals.
1. PERCEPTION : is a surface level phenomena in
which elicitor from the pathogen are recognized by
host receptor.
2. SIGNALLING
3. RESPONSE

10. PERCEPTION
• Perception means how pathogen and host recoginize
each other. It may take place directly or indirectly.
• After evaluation of numerous physiological,
biochemical and genetic experiments, different
models have gained importance as the basis for all
models is the gene-for-gene relationship between
host and pathogen for triggering race-specific
resistance.
• –Direct interaction models
• –Indirect interaction models

11. GENE FOR GENE HYPOTHESIS
• Flor (1946,47) showed correlation between
inheritance of pathogenicity and resistance
to linseed rust caused by Melampsora lini
which is now commonly known as gene -for
-gene hypothesis.
• that “for each gene conditioning rust
reaction in the host there is a specific gene
conditioning pathogenicity in the parasite.
• Gene for gene hypothesis does not address
the actual nature of the process, structure
and substances participating in the signal
transduction.

12. DIRECT INTERACTION MODELS
• four models have been proposed to demonstrate the
nature of recognition reaction and the expression of
the defense reaction:
• –The Elicitor- Receptor model
• –The Dimer Model
• –The Ion Channel defense model
• –The Suppressor- receptor model.

13. Elicitor-Receptor Model
(Albersheim et al., 1981)
• This hypothesis involve the two gene group system of
plant genes,
• where one gene act as a sensor within the signal-sensor
reaction that help in pathogen recognition
• Second group of several genes that express the plant
defense reactions
• However, this model does not explain how the
recognition by the plant turns on expression of the plant
dense genes.

14. • Drawbacks: the elicitor receptor model specifies
neither the structure of the corresponding
receptor nor does it define the nature and
mechanism of action of the effectors.

15. SUPRESSOR RECEPTOR MODEL
• Model was extended by Bushnell and Rowell (1981) and Heath
(1982).
• •It is based on the fact that all plants are susceptible to attack of any
pathogen and hence plant exhibit basic compatibility. However,
basic compatibility is conteracted by a general elicitor produced by
all pathogen which releases unspecific basic resistance.
• •In order to colonize a particular plant the homologous pathogen
has to produce specific suppressor to block the action of general
elicitor i.e. pathogen blocks secondarily its own elicitor of basic
resistance.
• •It assumes that active basic resistance is triggered unspecifically by
general acting elicitors produced by all pathogens is like wise
recognized by receptors present in all plants.

17. • However, part pathogen become compatible with certain
plant species because of mutation, the pathogen produces
a species specific suppressor that prevents its general
elicitor from acting on plant receptor or block elicitor
receptor interaction in other way, disturbing subsequent
signal transduction, or hindering formation or action of
effector.
• •In short, basic resistance would be prevented by specific
suppressor produced by pathogens thus allowing basic
compatibility
• –thus Bailey described this as elicitor/specific
suppression, to counteract to the release of active basic
resistance by a specifically acting elicitor.

18. INDIRECT MODELS OF INTERACTIONS
• Lack of evidence for a direct interaction indicated the
involvement of some other type of interaction
between the R gene and Avr gene products and this
lead to the concept of indirect interaction models
leading to resistance.
• lack of evidence for a direct interaction indicated the
involvement of some other type of interaction
between the R gene and Avr gene products and led to
the formation of the guard hypothesis.

19. GUARD HYPOTHESIS Vander
Biezen and Jones, 1998
• This model proposes that the R proteins interact, or
guard, a protein known as the guardee, which is the
target of the Avr protein. When it detects interference
with the guardee protein, it activates resistance.
• No direct interaction is found between Avr factor and
R proteins except shown in Avr pto-pto and Avr pita-
pita

21. • Arabidopsis RPM1 is a peripheral plasma membrane
NB-LRR protein. It is activated by either the AvrRpm1 or
the AvrB effector proteins. AvrRpm1 enhances the
virulence of some P. syringae strains on Arabidopsis as
does AvrB on soybeans. AvrRpm1 and AvrB are
modified by eukaryote-specific acylation once delivered
into the cell by the type III secretion system (red syringe)
and are thus targeted to the plasma membrane. The
biochemical functions of AvrRpm1 and AvrB are
unknown, although they target RIN4, which becomes
phosphorylated (1P), and activate RPM1. In the absence
of RPM1, AvrRpm1 and AvrB presumably act on RIN4
and other targets to contribute to virulence.

22. CONCLUSION
The interaction between plant and pathogen are
specific, complex and dynamic.
 Signals for activation of various defenses initiate in
response to recognition.
The outcome of interaction dependent on initial
sensing of the other organism via exchange of
molecular signal through signaling cascade and
modified gene expression.
Recognition is the first step by which response is
generated which is involved in defense signal
transduction.