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CREDIT SEMINAR
ON
Gene-For-Gene hypothesis and its validItY in THE present SCENARIO
Department of Crop Improvement
Speaker:Nimit KumarA-2012-40-006Ph.D Student
CSK HIMACHAL PRADESH KRISHI VISHVAVIDYALAYA
Disease Triangle
Disease Development
Conditions for disease :Host should be susceptiblePathogen should be virulentEnvironment should be favourable for the disease
What is Resistance…..? The ability of an organism to exclude or overcome, completely or in
some degree, the effect of a pathogen or other damaging factor
Vertical resistance
Horizontal Resistance
Two types
Basis of Disease resistance
ComponentsR genes
Avr genes
Interaction (Host Pathogen Interaction)
R GenesPresent in host plantControl a major step in the recognition of the pathogen and play a major role in expression of resistance
Control Gene-for-Gene interaction
R gene product inactivate toxin
Avr GenesAvr genes were first identified by H. H. Flor in 1950
Mild genes of pathogenResponsible for activation of certain defense response in host
Lead to resistance including hypersensitive response
PathogenAvr Gene
Plant
R Gene
Resistance Responses incl. the
HR
ELICITOR
(Gururani et al. 2012)
Examples of Avr genes and corresponding R- genes
Plants Avirulent gene Pathogen Matching R genes
References
Rice AvrPITA Magnaporthe grisea Pi-ta Valent (1998)
Tomato AvrPto Pseudomonas syringae pv. tomato
Prf Salmeron et. al. (1996)
Tomato AvrRpp8 Meloidogyne incognita and Macrosiphum euphorbia
Mi Milligan et. al. (1998)Rossi et. al. (1998)
Potato Coat protein Potato virus X (PVX) Rx Bendahmane et. al. (1999)
Potato Elicitin or AvrD Phytophthora infestans Pto Cai et. al. (2001)
Tobacco Replicase Tobacco mosaic virus(TMV)
N Whitham et. al. (1994)
Gene-for-Gene ConceptFor each resistance gene in the host there is a corresponding gene for avirulence in the pathogen conferring resistance and viceversa
H.H. Flor (1955)
H. H. Flor (1900 –1991)(MS 1924, Ph.D 1929)
H. H. Flor conducted studies with flax (Linum usitatissimum) and the flax rust pathogen (Melampsora lini)
------ to understand the genetic basis of the interaction between resistance and
virulence.
Flor originated gene‐for‐gene theory based on observations from his experiments
------ making crosses between both plants and pathogens to determine the inheritance of resistance and avirulence
Gene-for-gene hypothesis Quadratic Check
(Agrios 2007)
Pathogen Avirulence (virulence) genes
Plant Resistance (susceptibility) genes
R (Resistant) r (susceptible)
A (Avirulent)
AR (-) Ar(+)
a (virulent) aR(+) ar(+) where, – = Resistance + = Susceptible
(Staskawicz et al. 1995)
Gene-for-gene hypothesisMultifactor Interactions
(Agrios 2007)
Avirulence/virulence
Resistance/susceptibility
R1 R2 r1 R2 R1r2 r1r2
A1A2 - - - +a1A2 - - + +A1a2 - + - +a1a2 + + + +
where, – = Resistance + = Susceptible
Molecular basis for gene-for gene-relationship
On the basis of molecular interactions involved in producing resistant/susceptible responses in the host, the gene-for-gene relationship may be classified into two general groups:
Incompatible reaction
Compatible reaction
Incompatible reaction Found in biotrophic pathogens (obligate parasites) and is associated with hypersensitive response of the host
Only one of the four combinations would lead to the resistant response since the products of R & A would recognize & interact with each other.
The product of alleles a & r are unable to recognize each other, & there is no interaction between them hence reaction of host becomes susceptible.
Plant Resistance /susceptibility genes
Pathogen Avirulence /virulence genes
A a
R Resistance Susceptible
r Susceptible Susceptible
Allele A of the virulence gene specifies avirulence.
Allele a of the virulence gene governs virulence.
Compatible reaction Found in heterotrophic pathogens (facultative parasites)
The allele for susceptibility of the host ( r) and those for virulence in the pathogen produce specific compound, which interact with each other to produce susceptible response.
one of the fours combinations would lead to susceptibility and rest lead to resistant.
Plant Resistance /susceptibility genes
Pathogen Avirulence /virulence genes
A a
R Resistance Resistance
r Resistance Susceptible
Allele A of the virulence gene specifies avirulence. Allele a of the virulence gene governs virulence.
2nd gene for gene hypothesisFlor’s gene –for- gene hypothesis is purely a
hypothesis of identities. The resistance gene in the host and the
corresponding virulence gene can be identified by this hypothesis.
But it does not tell us about the gene quality. A second gene –for -gene hypothesis, which is an extension of Flor’s hypothesis, tells us about the quality of genes.
The quality of resistance gene in the host determines the fitness of matching gene in the pathogen to survive, when this gene for virulence is unnecessary.
Unnecessary gene means- a gene for virulence in the pathogen population against which matching resistance gene in the host is not present.
Reciprocally, the fitness of the virulence gene in the parasite to survive when it is unnecessary determines the quality of matching resistance gene in the host.
For instance, there are ten or more genes in the host for resistance to late blight of potato, R1, R2, R3------------R10.
Of these, the first four R1---R4 have been well studied. These genes have not been found of equal importance and strength.
R4 has not been successfully used on its own by breeders although it has occasionally been used in combination with other genes.
The R1 gene has often been used alone and it has given protection to the varieties against blight. The difference between these R genes is that virulences on R4 preexisted in population of Phytophthora infestans whereas virulences on R1 don’t (Van der Plank, 1975).
The ratio for virulence between R1 and R4 genes has been found to differ significantly. Thus there is difference in the quality of resistance genes R1 and R4.
Expansion of gene-For-gene hypothesis
Concepts and hypothesis proposed after
R- Avr gene interaction
Direct Interaction
Indirect Interaction
Direct Interacti
on
Elicitor-Receptor
Model
Ion Channel Defense Model
Dimer Model
Suppressor Receptor
Model
DIFFERENT MODELS PROPOSED UNDER DIRECT INTERACTION
Elicitor-Receptor ModelrecognitionSignal gene
(Pathogen) Signal (elicitor)
Sensor (receptor) Sensor gene(plant)
RAvr
Membrane proteins "receptors”
Avirulence factor
Cytoplasmic membrane
Release of expression of defense genes, “active” defense by plant
(Albersheim et al. 1981)
Dimer ModelrecognitionSignal gene
(Pathogen)Single (elicitor) Sensor (receptor) Sensor
gene (plant)
RAvr
Regulator molecule“Dimer” Avirulence factor
Regulatory function
BLOCKING chains towards basic compatibility
(Ellingboe 1982 )
Ion Channel Defense Model
recognitionSignal gene(Pathogen)
Single (elicitor) Sensor (receptor) Sensor gene (plant)
RAvr
Protein closedOpen Avirulence factor
Hypersensitive or programmed cell death effect release of expression of defense genes in neighboring cells
(Gabriel and Rolfe 1990)
Transmembrane
Suppressor-Receptor model
Bushnell 1981
Indirect Models GUARD HYPOTHESIS According to it elicitor does not directly
interact with R genes or receptor. Avirulence coded factor first of all react with guardee protein which either directly or indirectly form a complex and encode R gene which activate defense reaction.
Guard Model
Applications of Gene-for-gene hypothesis
The source of pathogenic variability in pathogens
The mutability of resistance and virulence genes
Why host resistance is expressed under one set of conditions and not others
Prediction of putative genotypes
Cataloguing and storing of R genes in the form of plant seeds or cuttings and V genes in the form of pathogen strains
Management and deployment of resistance genes in space and time
Geographic distribution of R and V genes
contd…
Hm 1 gene in Maize (Johal and Briggs
1992)
Includes the maize gene Hm 1 conferring race specific resistance to race 1 of the fungus Cochliobolus carbonum(causing leaf spot of corn) producing host specific toxin, the HC toxin
First R gene to be located, isolated and sequenced in 1992
Molecular basis of disease resistance in Maize Maize gene Hm 1 Invasion
by pathogen
NADPH-Dependent HC-toxin
HC toxin reductase
(Johal and Briggs1992)
Encodes
Inactivates/
Detoxify
Prevents
Xa21 rice gene - Xanthomonas
oryzae pv. oryzae (causing bacterial blight)
(Ronald 1997)
Rice gene Xa21, conferring resistance to bacterial pathogen Xanthomonas oryzae pv. oryzae (causing bacterial blight)
Xa21 represents a novel class of plant disease R genes encoding a putative receptor kinase (RK)
MOLECULAR BASIS OF DISEASE RESISTANCE IN RICE
(Ronald 1997)
TMV -N gene Tobacco
(Dinesh et al. 1995)
N gene present in Tobacco confer resistance to the viral pathogen. The amino acid sequence of the encoded N protein contains domains (NBS-LRR) which suggest a role for N in signal transduction leading to HR
Work done in university• Saharan (1977) identified 11 races of Melampsora lini (I-8 to I-17
and I-43)• Dr. Basandrai (1994) evaluated flax genotypes for resistance to
rust (Melampsora lini), wilt (Fusarium oxysporum ) and powdery mildew (Oidium lini) with 139, 35 and 24 genotypes, respectively, being free of infection
Work going on in the department• Molecular characterization of rust resistance introgressed into
Linum usitatissimum L. from its wild and cultivated gene pool
Present research scenario at international level
ConclusionThe precision of management and
deployment of resistance genes has increased considerably after Flor’s hypothesis
Interactions between disease resistance (R) genes in plants and their corresponding pathogen avirulence (Avr) genes are the key determinants of whether a plant is susceptible or resistant to a pathogen attack
Evidence has emerged that gene-for-gene interactions in the perception of pathogenic invasions and development of acquired resistance in plants involve different molecular and biochemical transduction pathways, which are still poorly understood
The interaction between plant and pathogen are specific, complex and dynamic
Increased understanding of the molecular basis of disease resistance will not only answer basic biological questions on the mode of action of resistance genes, but will facilitate efforts to engineer crops for resistance to disease
contd…
The hazardous effect of fungicides, bactericides and insecticides, or their degradation products, on the environment and human health strongly necessitates the search for new harmless means of disease control…….and i.e. Development of resistant varieties.