1. MOLECULAR CHARACTERIZATION OF GENE FOR GENE
SYSTEMS IN PLANT- FUNGUS INTERACTION AND THE
APPLICATIONS OF AVIRULENCE GENES IN CONTROL OF
2. NON HOST RESISTANCE :
• Apple trees and tomato pathogens
• Powdery mildew on wheat (Blumeria graminis f. sp. tritici)
Disease is exception rather than rule
HORIZONTAL RESISTANCE :
• General resistance, quantitative resistance
• Incomplete resistance but durable
3. VERTICAL RESISTANCE :
• Race specific , qualitative resistance, differential resistance
• Complete resistance, not durable – high selection presssure
• Follow gene for gene system
PLANT VARIETY 1 2 PLANT VARIETY 1 2 3 4
A _ + A _ + + +
B + _ B + _ _ +
C _ + _ +
D + _ + _
4. Reaction of plants to attacks by various pathogens in relation to resistance of
5. Each gene that confers avirulence (Avr) to the pathogen there is a
corresponding gene in the host that confers resistance (R) to the host
and vice versa – H.H.Flor (1946)
RESISTANT OR SUSCEPTIBILITY GENES IN THE
VIRULENCE OR AVIRULENCE
GENE IN PATHOGEN
r ( susceptibility)
A (avirulent) dominant AR (-) Ar (+)
a ( virulent) recessive Ar (+) ar (+)
RESISTANCE (R) OR SUSCEPTIBILITY ( r) GENES
IN THE PLANT
R1 R2 R1 r2 r1 R2 r1 r2
VIRULENCE (a) OR
GENES IN THE
A1 A2 - - - +
A1 a2 - - + +
a1 A2 - + - +
a1 a2 + + + +
10. Hydrophilic- lacking stretches of hydrophobic amino acids - enable
them to be anchored in cell membranes
May produced and localized in pathogen cytoplasm or secreted
through membrane pores
If secreted externally – directly acts as elicitors
If localized in cytoplasm of pathogen - acts indirectly as enzyme to
produce elicitor molecules
Acting as avirulence factors in elicitor-receptor model (plant
11. Contribution towards the virulence of pathogen. eg. AvrBs2 gene of
X. campestris pv. Vesicatoria
Avr proteins interact with specific plant proteins (virulence target) -
enhances availability of nutrients to pathogen .
Most R proteins contain amino acid leucine rich domain (LRR-
leucine rich repeats),
Depending on R protein LRR reside : cytoplasmic LRRs or
Leucine-rich repeats (LRR) region of R-genes is involved in
12. MAJOR CLASSES OF R PROTEINS
S. NO MAJOR R-GENE CLASSES EXAMPLE
1 NBS-LRR-TIR N, L6, RPP5
2 NBS-LRR-CC I2, RPS2, RPM1
3 LRR-TrD Cf-9, Cf-4, Cf-2
4 LRR-TrD-Kinase Xa21
5 TrD-CC RPW8
6 TIR-NBS-LRR-NLS- WRKY RRS1R
7 LRR-TrD-PEST-ECS Ve1, Ve2
8 Enzymatic R-genes Pto, Rpg1
LRR - Leucine rich repeats; NBS - Nucleotide-binding site; TIR -Toll/Interleukin-
1- receptors; CC - Coiled coil; TrD –Transmembrane domain; PEST -Amino acid
domain; ECS - Endocytosis cell signaling domain; NLS - Nuclear localization
signal; WRKY -Amino acid domain; HC toxin reductase - Helminthosporium
carbonum toxin reductase enzyme.
15. Plant proteins belonging to
the nucleotide-binding site–
leucine-rich repeat (NBS-
LRR) family are used for
Signal to cell
Response Defense protein
Diagram of a plant disease resistance protein in action. A portion of the protein
(MAROON) lies outside the cell and specifically recognises the harmful organism.
The remaining portion of the protein (RED) resides inside the cell and
communicates a signal to the plant’s genetic material, which in turn stimulates a
defense response against the invading organism.
16. • INDIRECT PERCEPTION OF AVR PROTEINS:
Protease dependent defense elicitation model
The co-receptor model
The guard hypothesis
The decoy hypothesis
Bait and Switch model
•DIRECT PERCEPTION OF AVR PROTEINS :
Elicitor- receptor model
17. Albersheim and Anderson Prouty, 1975 proposed this model.
Avirulence (Avr) gene of a pathogen encodes an elicitor (Avr) protein
that is recognized by a receptor protein encoded by the matching
resistance (R) gene of the host plant.
eg. Pi-ta R gene from rice and AvrPi-ta from Magnaporthe grisea
ELICITOR– RECEPTOR MODEL
18. PROTEASE DEPENDENT DEFENSE ELICITATION
Kruger et al., 2002 proposed this model.
eg.Tomato leaf mold –Cladosporium fulvum interaction.
Rcr3 required for Cf-2 mediated resistance towards C.fulvum
strains carrying Avr2, encodes a tomato cysteine endoprotease.
Rcr3 might process Avr2 to generate a mature ligand, or Rcr3
might degrade Avr2 - releasing active elicitor peptides that
interact with the extracellular LRR of Cf2.
20. THE CO-RECEPTOR MODEL
Jones and Jones,1996 proposed this model.
RPS5 an Arabidopsis NB-LRR protein localized to a membrane
fraction - activated by the AvrPphB cysteine protease effector from P.
AvrPphB is cleaved, acylated and delivered to the host plasma
membrane. Activated AvrPphB cleaves the Arabidopsis PBS1 serine-
threonine protein kinase, leading to RPS5 activation.
22. THE GUARD HYPOTHESIS
Van-der-biezen and Jones, 1998 proposed this model.
Interaction between guardee and Avr is recognized by the R
eg. AvrPto of Pseudomonas syringae and Pto gene of tomato,
Prf gene act as guardee.
Evolutionary unstable situation
R protein is absent -evolution of the guardee to avoid binding
R protein is present - selection will favor binding
24. Van der Hoorn and Kamoun, 2008 proposed this model.
Host protein termed as “decoy” - specializes in perception of the
effector by the R protein
Not contributing pathogen ﬁtness in the absence of its cognate R
Effector target monitored by the R protein is a decoy that mimics
the operative effector target
e.g. AvrPto and AvrBs3 - some host targets of effectors act as
decoys to detect pathogen effectors via R proteins
26. Peter Moffett , proposed this model in 2002.
The NB-LRR protein - primed (signaling competent) but
autoinhibited (restrained from signaling) state.
Functional nucleotide binding pocket and multiple intramolecular
interactions - fine-tuned balance between the LRR and ARC2.
Avr protein is brought into the NB-LRR system via the bait protein
- direct binding or alteration to bait.
Conformational changes within the nucleotide binding pocket-
allow signaling motif - downstream signaling components.
Subsequent to signaling, intramolecular interactions within the NB-
LRR protein dissociated.
BAIT AND SWITCH MODEL
44. FLAX RUST –
All the virulent rust strains retain intact copies of the Avr genes
(AvrL567) but have altered their sequences
Host R genes imposed selection for new variants to escape recognition.
Jones & Dangl (2006)
47. Functional genomic tools to disease resistance - interactions between
defense signaling and other plant processes.
Structural basis of recognition will enable us - design R proteins that
recognize essential virulence factors
New transgenic resistant plants by exploiting both avirulence genes
and resistance genes in molecular resistance breeding
Using avirulence gene products / race-specific elicitors - events in
signal transduction pathways can be studied.