Gene for Gene Hypothesis and Concept of Vertical and Horizontal Resistance

1. College of Horticulture, OUAT,
Chiplima
GENE FOR GENE HYPOTHESIS AND CONCEPT OF
VERTICAL AND HORIZONTAL RESISTANCE

2. “
For each resistance gene in the host there is
a corresponding gene for avirulence in the
pathogen conferring resistance and viceversa.

3. States that during their evolution host and parasite
developed complementary genicsystems
•Flor (1946,47) showed correlation between inheritance
of pathogenicity and resistance to linseed rust caused
by Melampsora lini which is now 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.
The concept has been applied with varying degree of proof to
other host pathogen combinations including viruses, bacteria,
fungi, nematodes, insects and a flowering plant (Orobanche).

4. Gene for
Gene Concept
H.H. Flor
Pathogen
genotype
Host genotype
R1 r1
Avr1
- +
avr1
+ +
-= Incompatible reaction
+= Compatible reaction
“for each gene
conditioning rust
reaction in the host
there is a specific gene
conditioning
pathogenicity in the
parasite”

5. PATHOGEN/HOST
 A1A2
 A1a2
 a1A2
 a1a2
 (Source:
Agrios,
R1R2 R1r2 r1R2 r1r2
- - - +
- - + +
- + - +
+ ++ +
2006. Plant Pathology)

6.  All the parasites in which gene for gene relationship
has been proved are essentially biotrophic or
biotrophs at least for some time after start of
infection
 (Xanthomonas campestris pv. malvacearum,
Phytophthora infestans, Venturia inaequalis (Vander
Plank, 1978).
 The genes-for-gene systems thus involve biotrophy.
 But the converse is not necessarily true. For example,
Plamodiophora brassicae , the cause of club root of
crucifers, is biotrophic but no evidence has yet been
presented in the literature to suggest that host-
pathogen interaction in them is based on a gene-for –
gene systems

7. A 1
a 1
P a t h o g e n
p r o d u c e s n o
s p e c i f i c
e l i c i t o r
P a t h o g e n
p r o d u c e s
a v r A 1 g e n e
p r o d u c t
( e l i c i t o r )
H o s t ( H a s g e n e r a l r e s i s t a n c e g e n e s
a n d s p e c i f i c r e s i s t a n c e ( R 1 ) o r l a c k o f
r e s i s t a n c e ( r 1 ) g e n e s )
R 1 g e n e - c o d e d h o s t r e c e p t o r
r e c o g n i z e s p a t h o g e n e l i c i t o r
m o l e c u l e s a n d t r i g g e r s d e f e n s e
r e a c t i o n s .
H o s t r e s i s t a n t
A 1 R 1
R 1 g e n e - c o d e d r e c e p t o r f i n d s
n o e l i c i t o r t o r e c o g n i z e , s o n o
d e f e n s e r e a c t i o n i s t r i g g e r e d .
V i r u l e n c e g e n e s o p e r a t e .
H o s t s u s c e p t i b l e .
H o s t l a c k s r e c e p t o r f o r e l i c i t o r .
N o d e f e n s e r e a c t i o n s t r i g g e r e d .
H o s t l a c k s r e s i s t a n c e t o t h i s
p a t h o g e n ’ s v i r u l e n c e g e n e s .
H o s t s u s c e p t i b l e .
P a t h o g e n
p r o d u c e s e l i c i t o r
a 1 R 1
N o p a t h o g e n e l i c i t o r p r o d u c e d
N o h o s t r e c e p t o r p r e s e n t
N o h o s t d e f e n s e r e a c t i o n s
t r i g g e r e d . H o s t l a c k s
r e s i s t a n c e t o t h i s p a t h o g e n ’ s
v i r u l e n c e g e n e s .
H o s t s u s c e p t i b l e
A 1 r 1
a 1 r 1
B a s i c i n t e r a c t i o n s o f p a t h o g e n a v i r u l e n c e ( A ) / v i r u l e n c ( a ) g e n e s w i t h h o s t r e s i s t a n c e
( R ) / s u s c p t i b i l t y ( r ) g e n e s i n a g e n e - f o r - g e n e r e l a t i o n s h i p , a n d t h e f i n a l o u t c o m e s o f
t h e i n t e r a c t i o n s .
HOW CAN WE EXPLAIN THIS
BIOCHEMICALLY?
P A T H O G E N ( H a s g e n e r a l p a t h o g e n i c i t y g e n e s a n d s p e c i f i c
a v i r u l e n c e ( A 1 ) o r v i r u l e n c e ( a 1 ) g e n e )

8.  There are two different schools of
thought pertaining to biochemical basis
of gene-for -gene interactions.
 According to first specificity in gene- for-
gene systems lies in susceptibility (Van der
Plank, 1978)
 whereas to other specificity lies in resistance
(Ellingboe, 1981).

9.  According to Van der Plank (1978), specificity in gene –
for- gene relationships lies in susceptibility.
 He explains it with the help of interactions of five host
and five pathogens attacking themspecifically.
 Suppose there are five host varieties with five
different R genes; R1, R2, R3----------R5. A plant with
resistance gene R1 is attacked by a pathogen having
virulence gene v1 and not to pathogen without this
particular resistance gene irrespective of how many
the virulence genes it mayhave.

10. Pathogen Plant
b
R1R1 R2R2 R3R3 R4R4 R5R5
v1v1
S R R R R
R S R R R
v2v2
R R S R R
v3v3
R R R S R
v4v4
R R R R S
v5v5
Table. The diagonal check for specificity in a gene-for gene relationship a
a. Plant reaction when resistance gene R1,R2,R3,R4,R5 at five loci
interact with virulence genes v1,v2,v3,v4,v5 at five loci in the
pathogen
b. Resistance is assumed to be dominant and RR can be replaced
by Rr. Virulence is assumed to be recessive. However, recessive
resistance and dominant virulence are also known.
R= resistant S= susceptible

11.  Vander Plank (1978) elaborated
protein for proteins hypothesis as a
biochemical explanation of gene for gene
interaction.
 The protein for protein hypothesis states that in
gene -for -gene diseases the mutual recognition
of host and pathogen is not by the genes
themselves but by their codedproteins.

12.  Vander Plank (1978) hypothesized that in susceptibility the
pathogen excretes a protein (virulence for product) into the
host cell which copolymenizes with a complementary host
protein (resistance gene product). This co-polymerization
interferes with one auto regulation of the host gene that codes
for the protein and by so doing turns the gene on to produce
more protein.
 In resistance, the protein specified by the gene for avirulence
in the pathogen and excreted into the host does not polymerize
with the protein coded for by the gene for resistance. It is not
recognized by the host at all.

13.  the biochemical explanation of gene for
gene systems is based on the fact that
specificity lies in resistance and not in
susceptibility as proposed by Vander
Plank (1978).

14.  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, which is an extension of Flor’s
hypothesis, tells us about the quality of
genes.

15.  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.

16.  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 andstrength.
 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. The difference between these R genes
is that virulences on R4 preexisted in population of Phytophthora
infestans whereas virulences on R1 don’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 andR4.

17.  The source of pathogenic variability in pathogens
set of
 The mutability of resistance and virulence genes
 Why host resistance is expressed under one
conditions and not others
 Prediction of putative genotypes
 Race nomenclature
 Genetic dissection of complex loci
 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 tome
 Detection of linkage and allelic relationship
 Geographic distribution of R and Vgenes
 Synthesis of multilines and multigene cultivars.

18. HISTORICAL OVERVIEW
Resistance in Mendelian fashion (Biffen, 1905)
Pathogenicity is inherited in Mendelian fashion (Newton,1929)
Correlation between inheritance of pathogenicity (Melampsora lini) and
resistance (Linseed) to (Flor , 1942, 1947, 1971) GENE FOR GENE HYPOTHESIS
Surface Carbohydrate elicitor - receptor model (Albersheim and Anderson Prouty, 1975)
Modified as elicitor- receptor model (Keen and Bruegger, 1977)
Protein- Protein interaction (Vanderplank, 1978)
Genetic and physiological evidences elicitor-receptor models (N T Keen ,1982)
Dimer Model (Ellingboe, 1982) Ion
channel defense model (Gabreil, 1984)

19. AvrPTO - PTO physically interact (Tang et. al, 1996 Scofield et al., 1996)
Guard hypothesis ( Van-der –biezen and Jones, 1998)
R proteins are dynamic and subject to intra-molecular interactions (Moffet et al., 2002)
Several host proteins as pathogen virulence targets were discovered (Mackney et
al. , 2003, Axtel et al., 2003, Rooney et al., 2005)
The soft wired model to explain the interaction of NBS-LRR domains (Bekhaldir et al.,
2004)
First Avr gene cloned from Pseudomonas syringae (Staskawicz et al., 1990)
First R gene (Hm1) was cloned (Johal and Briggs, 1992)
R gene (PTO) cloned (Martin, G.B. et al.,1993)

20. CONCEPT OF
VERTICAL AND
HORIZONTAL
RESISTANCE

21. Horizontal Resistance
to Plant Diseases
John Navazio
Organic Seed Alliance

22. Plant Disease Basics
 Pathogen – disease causing agent
 Disease - the resultant effects of parasitism by a
pathogen
 Resistance – any inherited characteristic of a host plant
which lessens the effects of parasitism
 Tolerance – parasitism is not impeded, but the host
suffers only marginal loss of yield and/or quality

23. How Do Pathogens
Cause Disease?
 All elements of the Disease Triangle are present;
Pathogen, Host, & Environment
 Pathogen must be present and reach the surface of the
host
 Pathogen must grow when environmental conditions are
favorable (establishment)
 Pathogen must colonize (colonization)
 Pathogen must reproduce (reproduction)

24.  The complexity of host–pathogen interaction makes it
difficult to categorize resistance into finite types.
 A large number of host–pathogen interaction systems
occur at various stages of coevolution.
 Resistance reactions may be generally categorized into
two major kinds – vertical or horizontal – based on their
epidemiological status and stability of resistance.
GENETICS OF INSECT
RESISTANCE

25.  The resistance is effective against all genotypes of the
parasite species without cultivar × isolate interaction (i.e.,
race-non-specific).
 Horizontal resistance is controlled by polygenes. Each of
the genes that condition the disease contributes toward the
level of resistance, and hence resistance is also called
minor gene resistance.
 Breeding polygenic resistance is more challenging. The
many minor genes cannot be individually identified and
consequently cannot be transferred through crossing in a
predictable fashion.
HORIZONTAL GENETICS OF
INSECT RESISTANCE

26. Vertical Resistance to Disease
 Term coined by Vanderplank in 1950s
 Vertical resistance is AKA “qualitative
resistance” or “race specific resistance”
 Almost always conferred by a single gene
 Each resistance gene usually confers
resistance to one race of the pathogen
 “Hypersensitive Reaction” is dramatic
 Easy to recognize and to screen for by
breeders
 These single genes almost always
“overcome” by new races of the pathogen

27.  This reaction is said to occur when a race of a pathogen
produces disease symptoms on some cultivars of a host
but fails to do so on others.
 This type of resistance is relatively easy to breed
because the major genes are easy to identify and
transfer through simple crosses.
 These genes control specific races or genotypes of pests
and hence do not protect against new races of the pests
VERTICAL GENETICS OF
RESISTANCE

28. Vertical – “All or None”

29. Horizontal Resistance to
Disease
 Term coined by Vanderplank in 1950s
 Horizontal resistance is AKA “quantitative
resistance” or “durable resistance”
 Always conferred by multiple genes
 Confers a level of resistance to all races
of the pathogen – also “new contact”
races
 It is a “rate reducing” process to the…
 establishment
 colonization
 reproduction
 It is equivalent to a “strong constitution”

30. Horizontal Resistance to
Disease
 Horizontal resistance (HR) is not complete
 The pathogen is able to survive – thereby it is possible
to have a stable ecological balance between the pest
and crop
 By allowing a number of races to survive, some more
virulent, some less virulent, then when they
intermate/genetic change there will be a wide range of
virulence in the population of the pathogen

31. Goode Thoughts
 “HR requires high management by the breeder of both
the pathogen and the host, but requires little by the
grower”
 “VR breeders and pathologists have been patching their
mistakes and bragging about how big their patches are!”
 Quotes from Dr. Jack Goode’s lectures in Plant
Pathology, Univ. of Arkansas, 1978

32. Horizontal Resistance – Graded with
Rank Order