HOST TARGET PROTEIN

2.  DEPART MENT OF GENETIC AND
PLANT BREEDING
 JANTAVADIC COLLEGE BARAUT
BAGPAT
 TOPIC = HostTarget Protein Mediated
Interaction And Source Of Disease
Resistance


3.  SUMMITED BY SUMMITEDTO
 Ranjeet kumar
 M.sc (Ag) 3rd 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.

7. 1. 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

8.  INDUCED DEFENCE
1. Programmed cell death (PCD)
2. Induced structural barriers
3. Phytoalexins
4. Pathogenesis related proteins (PR –proteins)
5. Post transcriptional gene silencing (PTGS)

9.  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

10.  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

11.  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.

12.  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.

13.  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

15.  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 ,

16.  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

17.  Arabidopsis RPM1 is a plasmaperipheral membrane NB-
LRR protein . It is activated by either the Avr 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.

18. 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.

19.  REFERANCE
 GOOGLE CROME
 SEARSLIDE
 THANKYOU