HOST TARGET.pptx ( RANJEET KUMAR MAURYA )

HOST TARGET PROTEIN

1. WELCOME

2. DEPART MENT OF GENETIC AND PLANT BREEDING JANTA VADIC COLLEGE BARAUT BAGPAT TOPIC = Host Target Protein Mediated Interaction And Source Of Disease Resistance

3. SUMMITED BY SUMMITED TO Ranjeet kumar M.sc (Ag) 3 rd sem . (220004242080 ) Dr. Amit Nagar Seassion 2023-24

4. HOST – PATHOGEN INTERACTION Disease is disfunction of normal physiological processes in plants caused by microorganisms or an abiotic factor. A pathogen that causes diseases in termed virulent A pathogen that does not cause diseases is termed avirulent Types of pathogen based 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 Programmed cell death (PCD) Induced structural barriers Phytoalexins Pathogenesis related proteins (PR –proteins) Post transcriptional gene silencing (PTGS)

8. PERCEPTION Perception means how pathogen and host recognize each other . It may place directly or indirectly . After evaluation of numbers physiological , biochemical and genetic experiments , differents modal have gained importance as the basis for all model is the gene for gene relationship between host and pathogen for triggering race specific resistance. Direct interaction models Indirect interaction model

9. GENE FOR GENE HYPOTHESIS Flor ( 146-47) showed correlation between inheritance of pathogenicity and resistance to linseed rust caused by Melampsora lini which is no 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 natural of the process, structure and substances participating in the signal transduction

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

11. Elicitor – Receptor Model ( Albersheim et al , 1981) This hypothesis involve the two gene group system of plant genes, Where one 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.

12. Drawbacks: The elicitor receptor model specifies neither the structure of the corresponding receptor nor does it define the nature and mechanism of the effectors. In short , basic resistance would be prevents 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

13. 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 product and this lead to the concept of indirect interaction models leading to resistance Lack of evidence for a direct interaction indicates 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 ,

14. GUARD HYPOTHESIS Vander Biezen and Jones 1998 This model proposes that the R protein 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 protein except shown in Avr pto - pto and Avr pita – pita

15. Arabidopsis RPM1 is a plasmaperipheral membrane NB- LRR protein . It is activated by either the A vr Rpm1 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 activat RPM1 .In the absence of RPM1, AvrRpm1 and AvrB presumably act on RIN4 and other targets to contribute to virulence.

16. 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 and modified gene expression. Recognition is the first step by which response is generated which is involved in defense signal transduction .

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