sheikh Mansoor shafi

Division of Biochemistry

SKUAST-J

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

Types of pathogen based on effects:

• Necrotrophy: plant cells are killed

• Biotrophy: plant cells remain alive

• Hemibiotrophy:plant cells initially alive and killed later

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.

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

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

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

PERCEPTION

• Perception means how pathogen and host recoginizeeach 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

GENE FOR GENE HYPOTHESIS

• Flor (1946,47) showed correlation between inheritance of pathogenicity and resistance to linseed rust caused by Melampsora liniwhich 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.

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.

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.

• 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.

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.

• 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.

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.

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

• 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.

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.