Nature and Genetics of Disease

resistance

Johar Singh
Dept of Plant Breeding and Genetics
Biological and economic effects of plant pests

Disease: a change from the state of metabolism necessary for the

normal development and functioning of an organism. Cause a reduction in
biological yield and invariably in economic yield.
Diseases/insect pests adversely affect plant growth/yield:
1 Complete plant death. Crop stand- reducing include those that cause
mildews, vascular wilts, insects such as cutworms (cause a seedling to fall over and
die).
2 Stunted growth. Viruses known to reduce metabolic performance of
plants without killing them outright. Usually cause severe reduction in
economic yield
3 Partial plant death. Only certain parts of the plant (e.g., branches)
are killed (e.g., in fungal diebacks).
4 Direct product damage. Some pests directly injure these products
completely (e.g., rotting of tissue) or reducing quality (e.g., causing blemishes,
holes).
 Control of plant parasites

Four strategies for controlling plant pathogens/pests:

1 Exclusion of pathogen from the host. Methods such as

legislation (quarantine, crop inspection), crop isolation to prevent
the pathogen from making initial contact with host plant.

2 Reduction or elimination of the pathogen’s inoculum. crop

rotation, sanitation (remove/burn) reduce spread of pathogen,
management practices (soil drainage, weeding, soil sterilization,
seed treatment) discourage growth,spread of parasites

3 Improvement of host resistance. Introduce genetic resistance .

4 Protection of the host. using chemicals (pesticides). Widely

used, environmentally unsafe, expensive.
 Resistance breeding (Concept)
Breeding for resistance to biotic stresses involves the manipulation of two genetic
systems – for host and for the parasite– not independently, but with regard to the
interaction between the two systems.
Degrees of resistance. Breeders arbitrarily set susceptibility–resistance scale.
True disease resistance has genetic basis. It is manifested in two basic forms:
Inhibition of infection or inhibition of subsequent growth of the pathogen.
•Resistance can be a qualitative or quantitative trait.
•The development and use of resistant cultivars has several advantages
Relatively inexpensive to deploy
No adverse environmental consequences
Convenient for farmers to use
Requires no additional production costs or decision-making during the crop season.
 Concepts of pathogen and host
Pathogen: living organism capable of inflicting a distinct disease or disorder in another
organism (the host).

Pathogenecity: Capacity of pathogen to cause disease or disorder in member of host species.

Virulence: The extent of disorder or disease development.

Pathogenecity and virulence of a pathogen vary among pathogen types (races or pathotypes).

Avirulent: Races/pathoypes that fail to successfully attack a given host.

Disease triangle: Pathogen + susceptible host + favourable environment = Disease

Pathotypes or races of pathogens may also be described in terms of aggressiveness/ non-

aggressiveness in relation to rate at which they produce disease symptoms.

Host -organism in which a pathogen may produce disease symptoms. Susceptible host in
which a pathotype/ race can cause a disease symptom.
 Defense Mechanisms

Broadly:
1 Pre-existing defense mechanisms .Include
morphological features that pose as barriers to the
penetration of the pathogen into the plant (e.g., presence
of lignin, cork layer, callose layers), or secondary
metabolites (phenols, alkaloids, glycosides) that have
antimicrobial properties.

2 Infection-induced defense mechanisms. Upon infection,

the host quickly produces chemical products (e.g.,
peroxidases, hydrolases, phytoalexins, etc.) to combat the
infection.
 Mechanisms of defense in plants against pests
Avoidance: Reduces the probability of contact between pathogens or insect
pests and the plant. It operates prior to the establishment of any intimate
host–pest/pathogen contact.
Antixenosis/non-preference) Rare in pathogens; primarily applicable to insect
pests.
A plant using this mechanism has characteristics (morphological or chemical)
that make it unattractive to insects for feeding, oviposition, or shelter.
In cabbage, a variant leaf color makes the plant unattractive to the cabbage
aphid, Pubescence in cotton prevents oviposition in the cotton boll weevil.
In cotton, a repulsive odour deters boll weevil from feeding on the plant.
Avoidance or non-preference may not be effective if there are no alternative
hosts.
Non-preference conditioned by allelochemicals is not effective with
monocropping and break- down of resistance are common. However,
morphological traits that interfere with feeding and breeding of insects are
important breeding goals as a first line of defense against insect pests.
Timing planting of crop (early or late planting) so that the susceptible growth
stage escapes the time when the insect pest is most abundant.
 Defense Mechanisms
Resistance :
•Resistance manifests after a host has been attacked
-curtail the invasion or reduce the growth and/or development of
the pathogen.
* May be biochemical, physiological, anatomical, or morphological.
(in insect pests is antibiosis)
Resistance is relative term for capacity of a host to reduce
adverse effect of a pathogenic attack. Some genotypes are more
resistant than others with equal amount of initial inoculum.
Resistance mechanisms may be pre-existing (passive resistance)
or induced/activated (active resistance) Resistance reactions
maybe hyper sensitive, overdevelopment,or underdevelopment.
 Plant defense
Tolerance: Tolerance (or endurance) operates to reduce the extent of damage inflicted.

The afflicted host attempts to perform normally in spite of the biotic stress. A host
may be highly susceptible (i.e., support a high population of pathogens or pests) and yet
exhibit little reduction in economic yield.

The mechanism may be applied to a situation in which a plant recovers quickly following a
pest attack such as grazing.

From the point of view of virologists, plants with few or no symptoms are described as
tolerant.

Exact mechanism(s) of tolerance not understood. May be due to plant vigour,

compensatory growth, and changes in photosynthate partitioning, among other factors.
 Specificity of defense mechanisms
• Almost all plant species are non-hosts for almost all parasites.

• Most avoidance mechanisms are non-specific (general or broad)

in that they are capable of avoiding groups of parasites with
similar ecological requirements, eg. the closed flowering habit
of some barley cultivars that excludes pathogens that invade
through the open flower, such as Ustilago nuda (loose smut),
also excludes Claviceps purpurea (ergot).

• However, some specificity may occur in the case of certain

repellents.

• Resistance mechanisms may also be specific or non-specific.

• Specificity may not only be at the pathogen level but even at

the race level (cultivar × race interaction).
 Genetic resistance
 Vertical resistance: Also known as
hypersensitivity, race- or pathotype-specific
resistance, major gene or oligogenic resistance, non-
durable or qualitative resistance, and non-uniform
resistance.
 VR :-race of a pathogen produces disease symptoms
on some cultivars of a host, but fails to do so on
others i.e., there is complete resistance in some
genotypes while others are susceptible.
 Vertical resistance is a differential resistance, or a
host × isolate interaction of cultivars against
different races of a pathogen.
 Vertical resistance …..
 Resistance is often absolute, conferring immunity against
the appropriate pathotype
 Delays start of epidemic, disappears when pathotype
virulent to VR gene prevalent.
 Relatively easy to breed : but may not be effective against
new races
 Monoculture, no crop rotation, populations of new strains
build up causing epidemic
 Disease/ insect resistance may be conditioned by dominant
or recessive genes. Dominant genes in resistance to, for
example, rusts, viruses, mildews, and nematodes.
 Vertical vs Horizontal Resistance

Resistance

Susceptibility

1 2 3 4 5 6
Races

Vertical Resistance to Races 2, 5, and 6

 Horizontal Resistance

Resistance

Susceptibility

1 2 3 4 5 6
Races

Horizontal Resistance to all Races

 Horizontal resistance…
Horizontal resistance: Also known as slow rusting, partial resistance, field
resistance, race-non-specific resistance, minor gene reactions, or polygenic
inheritance.

Lack of differential reaction of isolates on different cultivars. Resistance effective

against all genotypes of parasite species without cultivar × isolate interaction (i.e.,
race-non-specific).

Following initial establishment of pathogen, plant may resist its spread &
reproduction so that disease develops at a slower rate.

Evolution of new races absent under HR, making it more stable.

Controlled by polygenes. Each of genes that condition resistance contributes toward

level of resistance, also called minor gene resistance.

Polygenic resistance protects plants by slowing down the spread of disease and the
development of epidemics in the field.

Breeding polygenic resistance is more challenging. The many minor genes cannot be
individually identified
 Horizontal resitance…
Horizontal resistance may arise when:

(i)the host genes do not operate in a gene-for-gene fashion with the

pathogen genes (no differential interactions are possible); or

(ii)several to many host genes with small effects operate on gene-for-

gene basis with an equivalent number of genes in the pathogen population
(differential effects too small to be detectable, appear to be HR).

VR and HR may be viewed as extremes of a continuum, if one assumes that

gene-for-gene relationships are common in host-specific pathogen systems.

When few genes with large effects occur, differential interactions are
readily identified and the result is vertical resistance.

When more genes with smaller effects are involved, differential

interactions are less readily identified, resulting in a mixture of vertical
and horizontal resistance. When numerous genes of small effect are
involved, differential reactions cannot be discerned, & resistance is
primarily horizontal resistance.
 Durability of resistance
Important from plant breeders view point

Durable resistance - that remains effective in a widely grown

cultivar for a long time in environment that favours parasite.

Horizontal resistance is said to be durable whereas vertical

resistance is not. Adaptations of the parasite to newly introduced
resistant cultivars (i.e., breakdown of resistance) occurs frequently
in pathogens but less so in insect pests.

Such cultivars lack durable resistance.

Durability of resistance is variable even within pathosystems. For

example in one study involving resistance to stripe rust in wheat,
durability ranged from 1 to 18 years, depending on the cultivars.
 History of breeding for disease
resistance
Theophrastus (3RD Century): Cultivated variety differed in their ability to avoid
diseases.

Benedict Prevost: Diseases are produced by pathogen. He showed that wheat

bunt was produced by a fungus.

Andrew Knight (Mid 19TH Century):Crop varieties differed for disease

resistance.

Biffen(1905):Resistance to yellow rust in wheat was governed by a recessive

gene segregating in the ratio 3:1 in F 2.

Erikson (1894):Pathogens ,although morphologically similar,differed from each

other in their ability to attack different related host species.

Barrus (1911) :Different isolates of a microorganism differed in there ability to

attack different varieties of the same host species; this finding is the basis for
physiological races &/or pathotypes.

Flor (1956): Gene-for-Gene Hypothesis.

 Genetics of host–pathogen reactions

Genetics of resistance

R. H. Biffen first reported on the genetics of resistance. He reported that

resistance of wheat to stripe rust (Puccinia striiformis) was controlled by
a single gene. Since then many reports that much host resistance to
pathogens is simply inherited.

Dominance gene action is very common for resistance (especially

hypersensitive resistance). Monogenic recessive resistance is less common.
Polygenic resistance also known.

Genes may interact epistatically or additively. Commonly, resistance and

virulence genes usually operate on a gene-for-gene basis

Genes for resistance are often reported to be clustered in linkage groups.

Vertical resistance or race- specific resistance is oligogenic. The

inheritance of horizontal resistance is more complex.
 Gene-for-gene reactions
genetics of specificity
Working on flax rust (Melamspora lini), H. H. Flor discovered that the
major genes for resistance in the host interacted specifically with major
genes for avirulence in the fungus.

He proposed the gene-for- gene concept that states that for each gene
conditioning resistance in the host, there is a specific gene conditioning
virulence in the parasite.

In other words, a resistance gene can act only if a locus in the pathogen
carries a matching allele for avirulence.

By themselves, resistance genes are ineffective if pathogen carries the

appropriate allele for virulence (usually recessive).

Specific interaction occurs between dominant resistance alleles and the

dominant avirulence alleles .
 Gene for gene hypothesis
 Biffen (1905) resistance against yellow rust of wheat var “RIVET” was due to a single
recessive gene.

 Considerable confusion -----even with genetically stable wheat lines, reaction to rust
differed between locations and years. Artificial infection with spores collected from
the field resulted in inconsistent data .

 Confusion about variability could be cleared after discovery and characterization of

defined pathogen races.

 Differential reaction of a variety with a resistance gene towards particular races of

pathogen suggested there was genetic variability in pathogen which specifically
interacted with monogenic resistances in plant.

 Ausemus et al (1946) described three dominant monogenic resistances against the

wheat leaf rust and five dominat genes against stem rust .

 Pathosystems such as barley or wheat powdery mildew, flax rust, potato late blight
revealed that dominant monogenic resistance were quite common.

 Such resistance genes were the basis for Flor’s analysis of resistance.
 Gene for gene hypothesis
H.H.Flor analysed the genetics of a resistance interaction between flax
(Linum usitatissimum) and flax rust (Melampsora lini) and formulated
the gene for gene hypothesis (Flor 1942, 55, 71)

Infected flax lines carrying different resistance genes with F 2 progeny of

crosses between different races of rust pathogen. Tested for ability
to grow and multiply on more than 30 flax varieties carrying single
genes for rust reaction (Flor 1945).

Conclusion: Genetic factors of both plant and pathogen are required for
successful defense reaction of plant. Specificity of a plant-pathogen
interaction is determined by a dominant gene in pathogen and product
of resistance gene from plant.

Basis of plant resistance is therefore specific recognition between two

components.
 Gene for gene hypothesis
This recognition triggers further physiological defense
reactions resulting in hypersensitive cell death and
accumulation of molecules toxic to the pathogen. This is
also called a incompatible reaction between the plant and
pathogen.

Absence of either resistance gene product or avirulence

gene product, no recognition of the pathogen by the plant
leading to compatible reaction and susceptibility.

Mutation in either avirulence or resistance gene which

results in loss of function will result in a change from an
incompatible to a compatible interaction.
Resistance occurs only when a dominant R gene from the plant as well as
the dominant avirulence gene A from the pathogen are present. In all
other combinations, the interaction is compatible, resulting in
susceptibility.

Quadratic check with single locus in host and pathogen . Combination

of dominant resistant and dom avirulence results in resistance

HOST/PATH
OGEN RR/Rr rr

AA/Aa
- +
Avirulent
aa
+ +
virulent
 Pathogen
AVR avr

R- Incompatible Compatible
(Resistant) (Susceptible)
Host

rr Compatible Compatible
(Susceptible) (Susceptible)

Balint-Kurti lecture 1
Reciprocal check for two loci of resistance (R1 and r2) in two
cultivars.Cv1 and cv2 and corresponding two virulence loci in two
pathogen races (A1 and A2). Combination of R1 and A1 or R2 and A2
results in plant resistance. This reciprocal check defines a gene for
gene interaction

Cv 1 R1r2 CV2 r1R2

Race 1
A1a2
_ +

Race 2
a1A2 + -
 Pathogen
  AVR1AVR2 AVR1avr2 avr1AVR2 avr1avr2

R1-R2- Incompatible Incompatible Incompatible Compatible

(Resistant) (Resistant) (Resistant) (Susceptible)

 R1-r2r2  Incompatible Incompatible Compatible  Compatible

Host

(Resistant) (Resistant) (Susceptible) (Susceptible)

r1r1R2-  Incompatible Compatible  Incompatible Compatible

(Resistant) (Susceptible) (Resistant) (Susceptible)

r1r1r2r2 Compatible Compatible Compatible Compatible

(Susceptible) (Susceptible) (Susceptible) (Susceptible)

Balint-Kurti lecture 1
The presence of a resistance gene in host plant, exerts a strong selective
pressure for a mutation in the avirulence gene This selection pressure has
important consequences for the development of new pathogen races

Thus resistance in the gene for gene interaction is race specific whereas
susceptibility is not specific. The genetic basis of this specific resistance is best
understood by the quadratic check that can be used to describe the gene for
gene interaction

Resistance occurs only when a dominant R gene from the plant as well as the
dominant avirulence gene A from the pathogen are present. In all other
combinations, the interaction is compatible, resulting in susceptibility.

To prove a a gene for gene interaction, the quadratic check must be reciprocal,
i.e,.it must be true for at least two resistance genes in the host and two
matching avirulence genes in the pathogen (Vander plank 1973). If this condition
is fulfilled, a gene for gene interaction occurs in this particular disease.
Host pathogen combinations showing gene for
gene relationship
 Deviations from gene for gene
relationship
•Epistasis may be involved. This may be confused with complex parasitic
associations that occur in nature. Aberrant ratios may be due to
predisposition or preinduction of resistance by other pathogens

Some examples of deviation from strict gene for gene relationship are:

1. Two vir genes specific to a single resistance in flax rust, barley smut

2. Relationship between two interacting genes for resistance and two

interacting (duplicate) genes for virulence

3. A single R gene specified resistance to two different pathogens, eg. Wheat

gene Sr20 (stem rust) is identical to Lr15 (leaf rust), while Sr 24 is the same
as Lr19. Could be due to same/similar metabolic products conferring
resistance to two pathogens or due to very tight linkage.

4. In fusarium wilt of chickpea, multiple alleles have been reported for R

genes, which show phenotypic differences in resistance expression.
 Molecular basis of gene for gene hypothesis

• Pathogen Plant host cell

• A Avirulence gene →Resistance gene → Resistance

• B Compatible pathogen → resistance gene → Susceptible

• C Compatible pathogen → Susceptible host → Susceptible

• D Incompatible pathogen → susceptible Host → susceptible

Molecular model of gene for gene interactions (Staskawicz et al 1995).

• Resistance occurs only if there is a specific recognition between the resistance gene
product and product of matching avirulence gene (A ).

• In the absence of any recognition (B,C,D), no resistance reaction occurs and the
pathogen can colonise.

• Product of resistance gene in this model would be a receptor that actively

recognizes a direct/indirect product of avirulence gene.

• Only receptor ligand interaction results in specific recognition indicated by

hypersensitive response and disease resistance.
 Molecular basis of disease resitance
• A more molecular model derived from the observation of the dominant
character of both the avirulence gene and the resistance gene .

• The product of the resistance gene in this model would be a receptor that
actively recognizes a direct or indirect product of the avirulence gene. Only
the receptor ligand interaction results in specific recognition indicated by the
hypersensitive response and disease resistance.

• Physiological features such as K+/H+ exchange, rapid oxidative burst,

hypersensitivity at the site of infection, cross linking of plant cell walls,
synthesis of antimicrobial compounds known as phytoalexins, and induction of
pathogen-related proteins such as chitinases and glucanases represent some of
multiple metabolism turnover leading to disease resistance.
 Molecular basis of disease resitance

• During host invasion, pathogens release exogenous as well as endogenous

elicitors (Vorwerk et al. 2006; Huckelhoven 2007).

• Elicitors are molecules produced by either host or pathogen that in turn

induce a response by either host or pathogen.

• Fungal pathogen elicitors include enzymes which break down cuticle or

cell wall polysaccharides. Chitin, major constituent of fungal cell walls,
bacterial protein flagellin, cuticle and cell wall fragments are known to
be elicitor which trigger a defense response in plants.

• As these tissues are under physical or enzymatic attack, released

fragments are detected by R-proteins stationed in the cell membrane
and a defense response is initiated.

• Within 15 minutes of pathogen recognition, host cells begin producing

new proteins in reaction to the attack (Dangl and Jones 2001).
 Molecular basis of disease resitance

• This first response to invasion is known as a basal defense, and includes production
of proteins that inhibit pathogen enzymes, structural and chemical remodeling of the
host cell wall at penetration sites, and production of antimicrobial agents that will kill
the intruder.

• A second, more extreme, line of defense is HR, or programmed cell death (PCD),
where plant cell introduces toxic molecules into surroundings; creating a localized
environment incapable of sustaining life for both the pathogen and cell itself. HR is
efficient defense against many pathogens, but ineffective against necrotrophic fungi.

• Phytohormones as ethylene and jasmonate have been found to synergistically induce

expression of plant-defense genes in response to different pathogen attacks .
Exogenous application of methyl jasmonate to Arabidopsis plants reduces disease
development after infection by several fungi, such as A. brassicicola, B. cinerea, and
P. cucumerina
 SIGNAL PERCEPTION AND DEFENSE
ACTIVATION
The first process in signal transduction is the perception of an extracellular signal and its
transmission via the plasma membrane, resulting in accumulation of intracellular signaling molecules
and induction of a phosphorylation/dephosphorylation cascade, a cue system for the activation of R
gene expression.

Plant recognition of pathogens is mediated by large families of highly polymorphic R genes. The
products of these genes function to recognize directly or indirectly the products of pathogen-
encoded Avr genes

The majority of the identified R genes encode for intracellular proteins containing a predicted
nucleotide binding site (NBS) followed by a series of leucine-rich repeats (LRR) at their C termini
(http://pgfsun.ucdavis.edu/niblrrs/At_Rgenes/), although some R genes are notably different.

NBS-LRR resistance proteins generally contain one of two types of N-terminal domains. These are
either a domain that has homology with the Toll and Interleukin-1 Receptor proteins (TIR) or a
predicted coiled-coil domain (CC).

Studies of resistance proteins have indicated that the highly variable LRR domains determine
recognition of the pathogen Avr products (Dodds et al., 2001; Ellis et al., 1999; Jia et al., 2000),
whereas the more conserved TIR- NBS or CC-NBS regions are believed to propagate the
perception signal (Tao et al., 2000).
 HORMONAL PATHWAYS IN PLANT
DEFENSE (Emma Wanjiru Gachomo,etal 2003)

Phytohormones such as ethylene and jasmonate have been found to

synergistically induce expression of plant-defense genes in response to
different pathogen attacks (Penninckx et al., 1998). Exogenous application of
methyl jasmonate to Arabidopsis plants reduces disease development after
infection by several fungi, such as A. brassicicola, B. cinerea, and P.
cucumerina (Thomma et al., 2000).

Lorenzo et al. (2003) demonstrated that ERF1 (Ethylene response factor 1),
a downstream component of the ethylene-signaling pathway (Solano et al.,
1998), is an early ethylene- and jasmonate-responsive gene. They suggest
that ERF1 may be a common component of both ethylene and jasmonate
signaling pathways.
• Importance of salicylic acid (SA), jasmonates (JA), and ethylene(ET) as
primary signals in the regulation of plant defense is well established (Bari
and Jones, 2009; Pieterse et al., 2009). Pathogens that require a living host
(biotrophs) are commonly more sensitive to SA- mediated defense
responses, whereas pathogens that kill the host and feed on the contents
(necrotrophs) and herbivorous insects are generally affected by JA/ET-
mediated defenses (Glazebrook, 2005; HoweandJander, 2008).

• Changes in hormone concentration or sensitivity, such as triggered upon

interactions with biotic agents, activates a bouquet of hormone signaling
events that steers adaptive plant responses.

• The final outcome of the activated defense response is greatly influenced by

the composition and kinetics of the hormonal blend produced (De Vos et al.,
2005; Mur et al., 2006; Koornneef et al., 2008; Leon-Reyes et al., 2010).
• Different hormone signaling pathways act antagonistically or synergistically, thereby providing a
powerful regulatory potential to flexibly tailor the plant’s adaptive response to a variety of
environmental cues.

• Interaction between SA, JA, and ET signaling pathways emerged as an important regulatory
mechanism of plant immunity (Spoel and Dong, 2008; Grant and Jones, 2009; Pieterse et al., 2009).
Many studies have demonstrated that endogenously accumulating SA antagonizes JA-dependent
defenses, thereby prioritizing SA-dependent resistance over JA-dependent defense (Koornneef
and Pieterse, 2008). ET often plays a modulating role in this respect (Leon-Reyes et al., 2009,
2010; Zander et al., 2009). However, depending on the plant species and strategy of the attacker,
JA can also antagonize the SA pathway. For instance, in wild tobacco (Nicotiana attenuata) it was
demonstrated that the JA and ET bursts triggered by herbivore-derived elicitors, impede the SA
burst, resulting in tuning of the SA-JA signal interaction and hence the defense responses of the
plant to herbivory (Diezel et al., 2009).

• Recently, abscisic acid (ABA), auxins, gibberellins, and brassinosteroids emerged as forces on the
battle field as well. In many cases, these hormones interact antagonistically or synergistically with
the SA-JA-ET backbone of the plant immune signaling network, thereby redirecting its defense
output (Wang et al., 2007; Navarro et al., 2008; Yasuda et al., 2008; Campos et al., 2009; de
Torres-Zabala et al., 2009; Ton et al., 2009; De Vleesschauwer et al., 2010; Jiang et al.
 Boom and bust cycle
Priestley 1970
• New variety carrying VR resistant to prevalent pathotypes becomes
popular and occupies large growing area. This is period of Boom (high
popularity, large area) till a virulent pathotype develops or increases its
frequency to cause an epidemic. The popular variety looses popularity,
area declines , the variety is busted by the virulent pathotype

• Breeder develops a new variety with new VR genes resistant to prevalent

pathotype. This again goes a boom and bust cycle

• Selection pressure exerted on the pathogen by resistant variety is main

cause. Mutation may lead to new race which may be virulent on the VR
gene or virulent race which was in low frequency at the time of release
becomes more frequent
 Resistance breakdown
Breeders have successfully developed lines resistant to diseases by integrating R-
genes into their cultivars for many years; but a durable, long lasting resistance in
many cases has been difficult to achieve as pathogens quickly evolve and develop
counter resistance genes that circumvent the host cultivars resistance.

Breeders often spot this breakdown and hurriedly integrate a newly found effective
R- gene into their populations. In time, the new R-gene loses its effectiveness and
the boom- bust and induced co-evolution between crop and pathogen continues.

An example of this comes from the United States where in Indiana, 1955; a cultivar
was released that held on R-gene conferring resistance to Hessian fly ( Meyetiola
destructor ) attack. Just six years later the Hessian fly population had developed a
substantial amount of counter-resistance. By 1964, the Indiana breeders had
introduced a second R-gene into their cultivars. This new R-gene provided resistance
for eight years before counter-resistance developed. A third R-gene was introduced
and released in cultivars in 1971; and again was overcome by the pathogen, this time
in a period of ten years (Rausher 2001).
 Vertifolia effect
Vander plank 1963

• Named after a potato cultivar of this name, in which the effect was very pronounced.

• Vertifolia effect is a loss of HR which occurs during breeding for VR, later extended to include
loss of HR that occurs during breeding under protection of pesticides.

• level of HR can only be assessed by level of parasitism. If there is no parasitism because of a VR or a

pesticide, level of HR cannot be assessed. Because individual plants with a high level of HR are rather
rare in a mixed screening population, individuals with a low level of HR will be selected on the basis of
other attributes. loss is usually quite small in a single breeding cycle but, after many cycles can become
very serious .

• Example of vertifolia effect is loss of HR to potato blight (Phytophthora infestans) that has continued
ever since both the discovery of Bordeaux mixture in late 19 th century, and discovery of VR in 20th
century. A loss of HR to cotton pests has continued since discovery of DDT in the 1940s.

• Vertifolia effect is a very modern phenomenon. Its overall consequences are seen in the high levels of
HR in heritage cultivars, compared to modern cultivars. Main reason why heritage cultivars are so valued
by organic farmers.

• One of the main objectives of most amateur plant breeders will be to restore the horizontal resistances
that were lost to the vertifolia effect.
 Physiological races and pathotypes

• Concept of physiological races by Barrus {1908)

• Physiological races are strains of a single pathogen species differing in

their ability to attack different varieties of the same host species

• Varieties of host used to identify physiological races of a pathogen are

called differential hosts or host testers

• Differential hosts are chosen on basis of differences in their resistance to

pathogen, but genes for resistance present in them are usually not known

• Ideally each differential host should possess a single resistance gene

different from those present in others; such a set of differentials is known
as ideal differentials.

• A set of n differentials would identify 2n physiological races if there was

only two types of host-pathogen reaction eg., resistant and susceptible
 Contd… physiological races
• If more number of reaction types occur, eg., stem rust of wheat- the number of
identifiable races is rn.
• R= reaction types; n= number of ideal differentials
• Set of 18 ideal differentials available in linseed stem rust and 16 in late blight of
potato
• Identification of 4 physiological races of Tilletia sp causing wheat bunt with two
wheat differentials
___________________________________________________________
• Differential host Reaction to rust
» __________________________________________
Race I Race II Race II Race IV
• ____________________________________________________________
• Martin R R S S
• Turkey R S R S
• ___________________________________________________________
 Differentials
Differential hosts are sets of plant cultivars used to define
pathotypes of pathogens based on known susceptible and resistant
reactions.

Different varieties or lines with the same resistance gene(s) can

give the same reaction to a given race or strain of pathogen.
Therefore, the differential varieties or lines used by various
researchers may differ.
 Pathotypes

When the strains of a pathogen are classified on basis of virulence to known

resistance genes present in the host, they are referred to as pathotypes.

Ideal differentials are used to identify pathotypes

Pathotype classification more precise than of physiological races, as in

physiological races genes generally not known, and a differential host may
possess two or more resistance genes.

Pathotype classification is limited by availability of new resistance genes

and by the evolution of new pathotypes virulent to known resistance genes

Pathotype
An intra-subspecific classification of a pathogen distinguished from
others of the species by its pathogenicity on a specific host