R GENES

1. GENES IN PLANTS
Basavaraj kodsa
pg16agr8100

2. Time
Environment
Parasitism and Disease Development

3. How host plant defend pathogens
Pathogen
Defense barriers (waxy
cuticle, antimicrobial
compounds)
Recognition of conserved
structural patterns of
pathogens (PAMPs)
PTI
Effectors
Recognition of pathogens
effectors by R gene
proteins
ETI
Defense induced by
pathogen recognition

4. Host-pathogen co-evolution: Central dogma of Plant
Pathology
Kinase NBS TIR LRR Bent and Mackey (2007)
1
2
3
4

5. Plant immune system: zig zag model
PAMP Triggered Immunity (PTI) Effector Triggered Immunity(ETI)
Jones and Dangl (2006)

6. Effectors can be viewed as “Product
of parasite genes having phenotypic
expression in host bodies” (Dawkins
1999).

7. Specialized plant pathogens can evade or suppress this MAMP
triggered immunity (MTI) by secretion of virulence factors
called effectors.
A subset of these effectors, referred to as avirulence factors
(AVRs), which can be recognized by the resistance proteins
that trigger a second layer of host defense, referred to as
effector triggered immunity (ETI) or R-gene mediated defense.

8. The pioneering work on genetics of plant disease
resistance involving HR was done by Harold H. Flor in
linseed – Melampsora lini system (Flor 1956).
‘gene-for-gene hypothesis’

11.  Martin et al. (1993) provided first evidence of
direct interaction of tomato Pto gene with avrPto
from Pseudomonas syringae pv. tomato.
 Apart from direct interaction, evidences
indicate that R proteins also act as guard of a
specific component of the basic defense pathway.
Guard hypothesis:

12. Ex:Guard hypothesis
To date, the most convincing evidence for the guard hypothesis has
been found in Arabidopsis thaliana bacterial R-Avr systems where
RIN4 (RPM1- interacting protein 4) was identified as a cellular
protein that is required for the resistance to Pseudomonas syringae
pv. tomato mediated by RPM1 and RPS2.
The RIN4 (guardee) is modified in various ways, depending on the
Avr that it associates with, and these modifications then serve to
activate the corresponding R protein (guard).

13. “AVR-R gene interaction provides the
molecular basis for flor hypothesis and
Receptor-Effector interaction provides
the biochemical evidences for flor
hypothesis”

14. Molecular recognition in gene for
gene interaction

15. • When induced in timely manner, the concerted response efficiently
halt pathogen growth with minimal collateral damage to the plant
• No input is required from the farmer and no adverse environmental
effects
• Efficient reduction of pathogen growth
• Minimal damage to the host plant
• zero input of pesticides from the farmers and
• Most importantly the environment friendly nature of such crops.
Advantages of R gene

16. Disadvantages of R genes
• R genes are quickly defeated by co-evolving pathogens
• Many R genes recognise only a limited number of
pathogen strains
• R genes do not provide broad spectrum resistance
• Introgression of R genes into a elite cultivars by
convention breeding is a lengthy process

17. Classes of Plant Disease Resistance Genes Based on
Structural Features
Numerous R-genes identified, cloned and
characterized in different plants have been
categorized in eight classes (Table 1) based on
their amino acid organization.
(Gururani et al. 2012).

18. Classification of R gene
Based on structural feature (presence of certain Domains such
as LRR, NBS, TIR, etc)
Localization in the cell (Cytoplasmic, transmembrane or both)
Class Function Example
I Membrane associated, transcription regulating, Broad
spectrum
RPW8,
II Cytoplasmic, Signal transducing via Serine-Threonine
protein kinase
Pto
III Extra cellular LRRs and Transmembrane anchor Cf2 to Cf9
IV Extracellular LRR, transmembrane receptor, has
Cytoplasmic Serine- Threonine kinase (Signal transducing)
Xa21
V Cytoplasmic, membrane associated, LRR, NBS and TIR
domains
RPP5, N1,
L6, RRPP
VI Cytoplasmic, membrane associated, LRR, NBS, and a coiled
coil domains
RPM1,
RPS2

19. Structure and classes of plant disease
resistance genes

22. First R gene cloned was Hm1 in maize against race 1 of
Cochliobolus carbonum in 1992
But, Hm1 was disproved to be a resistance gene……………….
Because race 1 of C. carbonum produces the host specific HC
toxin and this is a pathogenisity factor and essential for
infection. Hm1 produce reductase enzyme which detoxifies the
HC toxin and thereby confers resistance against race 1……….
Therefore, logically the first R gene cloned and sequenced was
Pto in tomato which recognize the avrpto protein and thereby
activates the defence.

24. Plant pathogen interaction and development of disease
resistance
Gururani et al., 2012

25. How do R gene/protein functions
Pathogen
Nucleus
Alters the gene expression
Membrane bound
receptors-Effector interaction
Elicitors/effectors
Elicitors recognized by R protein
Activation
of defense

26. Functions of Resistance Genes
Signaling of plant stress hormones, generation
of reactive oxygen species (ROS),ethylene
biosynthesis, defense gene activation leading
to phytoalexin biosynthesis, cell wall
strengthening by the deposition of callose and
hypersensitive response
(Dixon et al. 2001)

27. Fungal pathogens and interacting R-genes
Gururani et al., 2012

28. Viral pathogens and interacting R-genes
Gururani et al., 2012

29. Cloned nematode resistance
genes
Gene Resistance gene
Hs1
(pro)
Resistance to cyst nematode Beta procumnence
Hi
(tomato)
Resistance to Meloidogyne incognita & Meloidogyne javanica
isolated fro tomatoes
Gpa2 Resistance to Globodera pallida identified In potato
Hero Resistance to Globodera isolated from tomato
Gro1-4 Resistance to Globodera rostochiensis

30. Nematodes and interacting R-genes

31. Evolution of R gene

32. Application of R genes
• RICE- BLAST ..IDENTIFIED Pi GENES
• PRH10-RES TO BLAST HAVING Pi54 and Piz5
• WHEAT- PGT….96000 genes identified.
• SR 26, SR 29 to tackle ug99 race…

33. Conclusion.