The concept of gene for gene hypothesis was first developed by Flor in 1956 based on his studies of host pathogen interaction in flax, for rust caused by Melampsora lini. The gene for gene hypothesis states that for each gene controlling resistance in the host, there is corresponding gene controlling pathogenicity in the pathogen. The resistance of host is governed by dominant genes and virulence of pathogen by recessive genes. The genotype of host and pathogen determine the disease reaction. When genes in host and pathogen match for all loci, then only the host will show susceptible reaction. If some gene loci remain unmatched, the host will show resistant reaction. Now gene – for –gene relationship has been reported in several other crops like potato, sorghum, wheat, etc. The gene for gene hypothesis is also known as “Flor Hypothesis.”
1. Gene for Gene Hypothesis
Speaker:
B.Rachana
RAD/2018-18
Ph.D 1st year
(GPBR)
GP-510 Breeding for Biotic and
Abiotic stress Resistance
2. Disease is an abnormal condition in an
organism produced by an organism or an
environmental factor.
Host is the plant affected by a disease.
Pathogen is the organism that produces the
disease on the host.
Environment refers to sum total of conditions
influencing the disease development.
3. Disease Development
Conditions for disease :
1. Host should be susceptible
2. Pathogen should be virulent
3. Environment should be favourable for the disease
DiseaseTriangle
4. What isResistance…..?
Theability of anorganismto excludeor overcome,completely or in
somedegree,the effect of apathogen or other damaging factor.
Vertical resistance
Horizontal Resistance
Twotypes of Resistance
6. R genes
o Present in host plant.
o Controls a major step in the
recognition of the pathogen and plays
a major role in expression of
resistance.
o Control Gene-for-Gene interaction.
o R gene product inactivates the toxin.
7. Avr Genes
o Avr genes were first identified by H. H.
Flor in 1950.
o Mild genes of pathogen.
o Responsible for activation of certain
defense response in host.
o Leads to resistance including
hypersensitive response.
10. 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)
11. Gene-for-Gene Concept
‘For each resistance gene in
the host there is a
corresponding gene for
avirulence in the pathogen
conferring resistance and
viceversa’
H.H.Flor (1955)
13. • 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 proposed 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.
14. Molecular basisforgene-forgene-
relationship
On the basis of molecular interactions involved in producing
resistant/susceptible responses in the host, the gene-for-gene
relationship maybeclassified into two generalgroups:
Incompatible reaction
Compatible reaction
15. Incompatiblereaction
Foundin biotrophic pathogens (obligate parasites) and is
associated with hypersensitive response of thehost.
Only one of the four combinations would lead to the resistant
response since the products of R & Avr would recognize&
interact with eachother.
Theproduct of alleles a & rare unable to recognize eachother,
& there is no interactionbetween them, hencereaction of host
becomessusceptible.
16. 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.
17. Foundin heterotrophicpathogens (facultative
parasites).
Theallele forsusceptibilityof thehost (r)and those for
virulencein thepathogenproducesspecificcompound,
whichinteractswith eachother to producesusceptible
response.
one of thefour combinationswould lead to
susceptibilityand restleadsto resistant.
Compatiblereaction
18. 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.
20. Flor’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 proposed
by Vanderplank, which is an extension of
Flor’s hypothesis, tells us about the quality
of genes.
Second Gene for Gene Hypothesis
21. 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.
22. Of these, the first four R1---R4 have been well
studied. These genes have not been found of
equal importanceand strength.
From the reports available in the literature, 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.
23. The difference between these R genes is that
virulences on R4 preexisted in population of
Phytophthora infestans whereas virulences on
R1 didn’t (Van derPlank, 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.
24. • 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.
• Cataloguing and storing of R genes in the
form of plant seeds or cuttings.
• Management and deployment of resistance
genes in space and time.
• Geographic distribution of R and V genes.
• Synthesis of multilines and multigene
cultivars.
Gene for Gene hypothesis is used to
study the following
26. • Genetic studies of the flax-flax rust
interaction led to the formulation of the
gene-for-gene hypothesis and identified
resistance genes (R) and pathogenicity genes,
including avirulence (Avr).
• R genes have been cloned from four of the
five loci in flax and all encode proteins of the
Toll, Interleukin-1receptor, R gene-nucleotide
binding site-leucine-rich repeat (TIR-NBS-LRR)
class.
• Avr genes have been cloned from four loci in
flax rust and encode small secreted proteins
with no close homologs.
27. The AvrL567 gene product is recognized in plant cells
by L5.
(a) The flax rust gene variant AvrL567-
A was modified for plant expression
using the CaMV 35S promoter and
nopaline synthase (Nos) and cloned for
Agrobacterium-mediated transient
plant transformation.
(b) Transient expression of AvrL567-A
induced a necrotic response in flax
leaves of the L5 genotype but not in
NIL leaves lacking L5, L6 or L7.
(c) The AvrL567-A protein would be
secreted in to the space between the
haustorial cell wall and invaginated
host cell plasmamembrane
(extrahaustorial matrix, EHM).
The secreted protein would then be
transported across the plant
membrane by an unidentified
mechanism and recognized by direct
interaction with the cytoplasmically
localized L5 protein.
28. • Avr proteins enter the host cell, have virulence
effector functions and in resistant host genotypes,
are recognized by direct and specific interaction
with host R proteins, leading to activation of rust
resistance defense responses.
• Direct interaction between R and Avr proteins is
the basis of gene for-gene specificity in the flax-flax
rust system.
• R and Avr genes have the signatures of diversifying
selection, suggesting the existence of a co-
evolutionary race between the host plant and its
obligate rust pathogen.
29.
30. • In maize, the leaf blight disease caused by the fungus Cochliobolus carbonum race
1 (CCR1) affects net yield potential and its asexual form (i.e., Helminthosporium
carbonum (HC)) is the most destructive biotic fungal pathogen at any stage of
development .
• In maize the R gene Hm1 provides complete protection against southern leaf blight
caused by CCR1.
• Hm1 was the first DR gene to be cloned, which disarms the pathogen directly
instead of participating in the plant recognition and response system as most DR
genes do.
• Apart from Hm1 gene, certain lines of maize contain a second DR gene named
Hm2, encodes a structurally truncated duplicate of Hm1.
• Both Hm1 and Hm2 encode nitrate reductases that detoxify the HC-toxin of CCR1 .
• Both these genes are different in two aspects;
1. Hm1 is completely dominant conferring absolute resistance to plants, whereas
Hm2 exhibits incomplete dominance.
2. Hm1 - absolute protection in all parts of the plant at all stages of development,
while Hm2 confers effective resistance only at maturity.
31. • The NADPH-dependent HC-toxin reductases (HCTR1
and 2) encoded by enzymatic class of disease resistance
homologous genes (Hm1 and Hm2) protect maize by
detoxifying a cyclic tetrapeptide, HC-toxin, secreted by
the fungus Cochliobolus carbonum race 1(CCR1).
Maize gene Hm 1 and HM2 Invasion by pathogen
NADPH-Dependent
HC toxin reductase Inactivates/Detoxify
HC-toxin
PreventsEncodes
32. Functional genomic tools to disease resistance – interactions
between defense signaling and other plant processes.
Structural basis ofrecognition willenableus - design
R proteins that recognize essential virulence factors.
New transgenic resistant plants by exploiting both
avirulence and resistance genes in molecular resistance
breeding.
Using avirulence gene products/race-specific signal
transduction pathways can be studied.
