Resistance Breeding UG - .pdf

Types of stress
Biotic
• Diseases
(Fungi, Bacteria, Virus, Nematodes)
• Insects
• Herbivores
• Other plants (weeds)
Abiotic
• Heat
• Cold
• Drought
• Salt
• Mineral deficit

Stress
(Biotic and abiotic)
Resistance Susceptibility Avoidance
Stress response

Resistance Breeding
• Resistance
Inherent ability of organism (plants) to resist or withstand the stress (biotic or
abiotic)
• Breeding
Allowing the multiplication or reproduction of desired genotype of plant

Concept of resistance in breeding
• Breeding for yield and other morphological traits (plant height, tillers, spike length, no. of grains per panicle etc.)
as well as breeding for resistance to abiotic stress, are conceptually different from breeding for resistance to
biotic stresses.
• Breeding in the former cases entails the manipulation of one genetic system – plants.
• Breeding for resistance to biotic stresses involves the manipulation of two genetic systems – one for plants (host)
and the other for the organism (pathogen/parasite) – not independently, but with regard to the interaction between
the two systems.
• The breeders need to understand the interrelationships between plants and their pathogen/parasites that have
persisted through co-evolution and co-existence.
Resistance
• Resistance is a response to a cause.
• There are degrees of resistance.
• In terms of disease, resistance is always relative to a benchmark.

• A genotype that is immune to a disease is completely or totally resistant to it.
• A resistant cultivar has less disease than the standard cultivar – it could be a little or a lot less
diseased.
• True disease resistance has a genetic basis and hence is amenable to plant breeding methodologies.
• It manifests in two basic forms: inhibition of infection or inhibition of subsequent growth of the
pathogen, the former being the more common form of resistance.
• Resistance can be a qualitative or quantitative trait.
• Breeding for pest resistance is an integral part of any system of crop pest control.
-A.L. Hooker
• If yield and other desirable traits maintained, resistance (host resistance) is an ideal method of
breeding to control plant pests.

Merits of resistant cultivars
• relatively inexpensive to deploy resistance and has no adverse environmental
consequences compared to other pests control methods.
• In addition, convenient for farmers to use, requiring no additional production costs or
decision-making during the production season.
Note: However, when host resistance is not satisfactory, farmers may need to
supplement host resistance with other pest management practices like use of pesticides.

Natural enemies (NE)
• Natural enemies are organisms that kill, decrease the
reproductive potential of, or otherwise reduce the numbers
of another organism.
• Eg. fungi, bacteria, virus, weeds, Insects, herbivores etc. act as
natural enemies of plants.

Classification of natural enemies and
the nature of their effects on plants
Taxonomic Classification Classification of NE Effect on plants
Viroid Pathogens Disease, Infection
Virus Pathogens Disease, Infection
Phytoplasm Pathogens Disease, Infection
Bacterium Pathogens Disease, Infection
Fungus Pathogens , Parasites Disease, Infection; Infestation
Vertebrate Herbivores Biting damage
Nematode Parasite Infestation
Mite Parasites Infestation
Insect Parasites, Herbivores Infestation, Biting damage
Snail and Slug Herbivores Infestation, Biting damage

Common terminologies
Disease: Physiological disturbance of a plant /part of a plant caused by a stress factor
or a combination of stress factors resulting in symptoms. eg. BLB in Rice, rust in
wheat
Host: Susceptible to a NE and serves both as source of nutrition and as living
substrate. eg. Plants (wheat, rice, tomato etc)
Parasite: Organism that more or less permanently and sometimes for part of its life
cycle lives in close connection with a living organism and withdraws its nutrients
completely or partially at the expense of that organism. Eg nematodes, mites
Pathogen: Having the capacity to infect plants; exploits the plants as a source of
nutrition. Eg. Pyricularia oryze, Phytopthera infestans

Infection: The use of a plant as nutrient source by a pathogen, usually resulting in
reproduction of that pathogen.
Infestation: The use of a plant as nutrient source by NE and may or may not live
on that plant. Eg. Insects, nematodes, mites
Sign: Visible parts or products of pest by which it can be recognized. Eg. Rust
spores, larvae, excreta of insect
Symptom: Deviation from normal growth and dev. of a plant by stress factor(s).
Eg. mosaic and mottling of leaves, stunting
Stress factor: Identifiable factor that potentially results in damage. Eg. Disease,
insects, heat, drought
Damage: Reduction in physical or economical yield of a crop due to stress factors.
Eg. Reduced plant height, decrease in yield

• Race: A group of genotypes within a pathogen species that is distinguished by
its virulence spectrum.
• Biotype: synonym of race but used for phytophagous insects and for parasitic
higher plants ( while in Nematode: pathotype)
• Forma specialis: Unit within the natural enemy species that is distinguished by
its host range; differ in pathogenicity (capacity of a microbial organism to infect
a plant species) but belong to the same pathogen species.
• Virulent: Pathogen genotypes to which the resistance is not effective.
• Avirulent: Pathogen genotypes to which the resistance is effective.
• Isolate: A sample of pathogen/parasite that is stored alive or maintained in
isolation on plants or in nutrient media.

Classification of Pathogens
According to their characteristics of the infection process
Biotrops: Withdraws nutrients from living host tissue. (viruses, PM, rust fungi, loose
smuts)
Necrotrops: Withdraws nutrients from tissues killed by natural enemy. (Septoria,
Helminthosporium)
Hemi-biotrophs: Withdraws nutrients from living host tissue that soon after this will
die. (Phytophthora infestans, DM)
Weakness pathogen: That only can infect weakened plant parts with reduced
fitness. (Botrytis, Pythium)
Vascular wilts: Pathogen that causes wilting of the host plant by blocking of the
xylem and lives in and spreads through the vascular tissue. (Fusarium, Verticillium)

Disease
• A physiological deviation from the normal functioning of the organism (i.e
crop plant) caused by pathogenic organisms is a disease and may be
caused by fungi, bacteria, or viruses
• An abnormal growth and development of the plant will cause a reduction
in biological yield and invariably in economic yield
• therefore, the need to control pathogens and insect pests in crop
production

Ways by which diseases and insect pest's affects plant:
Four basic ways by which diseases and insect pests adversely affect plant yield
and general performance, and, ultimately, reduce economic value
1. Complete plant death
• Certain parasites eventually kill the affected plant completely
• When this occurs early in crop production, gaps are left in the crop stand,
where plants in the vicinity cannot compensate for such gaps.
• Additional nutrients may become available to the existing plants due to
reduced competition, however, the reduced plant density results in reduced
biomass.
Eg, mildews, vascular wilts, and insects such as cutworms that cause a seedling
to fall over and die

2. Stunted growth
• Pests reduce the metabolic performance of plants without killing them
outright.
• Reduction in size of plant and its parts, and usually causes severely
reduced economic yield of plants
• Eg. Mealybug in rice, most viral infections
3. Partial plant death
• Some diseases that afflict adult plants don't/can't completely kill them.
• Rather, only certain parts of the plant (e.g., branches) are killed
• e.g. fungal diebacks

4. Direct product damage
• Above three effects of disease and pests, indirectly affect the economic
or harvested product if it is the fruit, seed, or modified organs (tubers,
bulbs).
• Some pests directly injure these products completely (e.g., by causing
rotting of tissue) or reducing quality (e.g., by causing blemishes, holes)
• Eg. Red rot of sugarcane, Helicoverpa infestation in tomato

Methods of control of plant pests (insect/disease/parasite)
Four strategies are available for controlling plant pathogens and pests:
1. Exclusion of pests from the host
• Methods such as legislation (plant quarantine, crop inspection) or crop isolation to
prevent the pathogen or pest from making initial contact with the host plant
• Quarantine prevent the introduction of new pathogens into a production region
• Such laws are commonly enforced at the points of entry for people and goods into a
country

2. Reduction or elimination of the pathogen’s inoculum
• If pathogen gains access into a production area, use of various methods to
remove it or reduce the inoculum to contain it.
• Method such as crop rotation reduces disease build up in the field, while
sanitation practice also reduces the spread of the pathogen.
• e.g., removing diseased plants and burning them
• The producer may also implement management practices that discourage the
growth and spread of parasites
• e.g., soil drainage, weeding, soil sterilization, seed treatment

3. Improvement of host resistance
• Concern to plant breeders
• requires breeding to introduce genetic resistance into adapted
cultivars.
4. Protection of the host
• using chemicals (pesticides)
• widely used, environmentally amicable and expensive

Concepts of pathogen and host
The pathogen
• Pathogen: living organism that is capable of causing a distinct disease or
disorder in another organism (the host)
• Pathogenicity: capacity of the pathogen to cause disease or disorder in a
member of a host species is its pathogenicity,
• Virulence: extent of disorder or disease development
• Pathogenicity and Virulence of a pathogen vary among pathogen types
(races or pathotypes).
• Races or pathotypes that fail to cause disease symptoms or successfully
attack a given host are called avirulent, while opposite is virulent.

• Only the presence of a pathogen on a susceptible host is not
enough to cause disease symptoms to occur.
• A third factor – favorable environment –is needed.
• Virulent Pathogen, susceptible host and favorable environment
referred to as the disease triangle.
• Pathotypes or races of pathogens may also be described in terms of
aggressiveness or non-aggressiveness in relation to the rate at
which they produce disease symptoms.

The host
• Host (genotype, plant) is the organism in which a pathogen may produce
disease symptoms.
• Susceptible host is one in which a pathotype or race can manifest a disease
symptom.
• A host may employ one of several mechanisms (defense mechanisms) to resist
pathogens.
• These mechanisms may be pre-existing or induced upon infection.

1 Pre-existing defense mechanisms
• 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

Principles underlying selection for disease
resistance
i) Sources of resistance must be identified from
existing materials: cultivar itself, commercial
cultivars, other varieties, land races, weedy
relatives, related species or genera.
ii) Screening technique for resistance by exposure to
the disease pathogen under natural or artificial
induced epiphytotic is necessary to distinguish
between resistance and susceptible plants.
iii) Mode and inheritance of resistance must be
understood.
iv) The resistance gene must be transferred to an
adapted cultivar.
v) Progeny testing of resistant plants to varify the
inherent nature of resistance

Disease development
The development of any disease depends on a
close interaction among three diverse factors
they are
I) the host: It should be suitable
II) II) the pathogen: It should be aggressive in
nature and
III) III) the environment: It should be favourable.

Types of plant pathogen
interaction
• Micro-organisms can form symbiotic
relationships with the host
• Micro-organisms may cause disease in
the host
• Host plant may be resistant to the
pathogen and no infection develops
• Host plant may show some tolerance to
infection

Different levels of plants' defence systems
• Anatomical: morphological and structural systems:
cuticle, bark, wax
• Pre-existing proteins and chemicals: anti microbial
proteins: phytoanticipins/phytoalexins: terpens,
phenolics, alkaloids, glycosides
• Inducible systems: (i) Elicitor response: molecules
released by pathogen are recognized by receptor like
molecules present in host/non host. (ii) General
response: PR proteins
• Systemic response: Systemic acquired resistance (SAR);
Messages are passed from sites of infection systemically
to other parts. SAR has two phases (initiation and
maintenance); Initiation phase: signal molecules (salicylic
acid) into phloem transported to target cells where SAR
genes (PR proteins) expressed. Then later on
maintenance.

Defence mechanisms
1. Avoidance: It reduces the chance of contact
between prospective host tissue or food plant
and a potential natural enemy usually as a result
of particular morphology, phenology or smell of
the potential host plant. Mimicry, camouflage,
thorns, hairs, spines, smell, colour, taste, repellent
odours are some of the examples.
2. Resistance: It is the ability of the host to reduce
the growth and or development of the parasite or
pathogen. It is of 2 types:

2.1 Race specific/vertical resistance/gene for gene
resistance: A resistance that is effective to specific
(avirulent) genotypes of a pathogen species.
2.2 Race non specific/horizontal resistance/no gene
for gene resistance: A resistance that is equally
effective to all the genotypes of a pathogen
species.

3. Tolerance: It neither restricts parasitic contact
nor the growth and development of the parasite
after establishment. As a consequence, it does
not affect the amount of damage/symptoms per
unit quantity of parasite present.
• Susceptibility: Incapacity of a plant to reduce the
growth, development and reproduction of the
natural enemy.
• Sensitivity: Character of the host plant to
develop relatively severe symptoms or severe
damage per unit quantity of the natural enemy.

Sensitivity = { (Yield without
pathogen -Yield with
pathogen)/ Yield without
pathogen}/ Con. of the
pathogen

Gene for gene relationship
• Flor 1956 based on his work on linseed rust
postulated the gene for gene relationship
between a host and pathogen. This
relationship states that" A resistance gene, R
is only effective if the infecting pathogen
carries the corresponding avirulence gene, A"

• Host resistance is conditioned by dominant
allele, R.
• In the pathogen, virulence is conditioned by
recessive allele, a.
• Resistance reaction occurs when
complementary genes in both host and
pathogen are dominant.
• A host genotype that caries no dominant alleles
at any of the loci is susceptible for all the races
of pathogen (even if avirunlent)
• 'A' avirunlent allele is dominant over 'a' virulent
allele and resistant allele 'R' is dominant over
susceptible allele 'r'.
• Compatibility depends on the genotype of the
host and the genotype of the pathogen.

Host
genotype
Pathogen
genotype
A a
R - +
r + +

Host
gen.
Pathogen genotypes
A1A2a3 a1A2a3 A1a2A3 a1a2A3 A1A2A3 a1A2A3 a1a2a3
r1r2r3
+ + + + + + +
R1r2r3
- + - + - + +
r1R2R3
- - - - - + +
R1R2r3
- - - + - - +
R1r2R3
- + - - - - +
r1r2R3
+ + - - - - +
R1R2R3
- - - - - - +

Classification of gene for gene relationship
(i) Incompatible reaction: The alleles for resistance
in the host (R) and those for avirulence in the
pathogen (A) produce specific compounds, which
recognize each other; when these specific
compounds interact, they produce resistant
response in the host. The alleles for susceptibility
(r) in the host as well as those for virulence (a) in
the pathogen either produce these compounds in a
modified state or do not produce them at all. The
products of alleles a and r are unable to recognize
each other, and there is no interaction between
them. The lack of interaction between the products
of the genes for resistance and pathogenicity
produces susceptible reaction in the host

(ii) Compatible reaction: Alleles for susceptibility (r)
in the host and those for virulences (a) in the
pathogen produce specific compounds, which
interact with each other to produce the susceptible
response. A lack of interaction between the
products of r and a genes specifies resistant
response of the host. The allele for resistance in the
host (R) produces a modified substance which is
unable to recognize and interact with the product
of the allele for virulence in the pathogen.
Similarly, the allele for avirulence in the pathogen
(A) specifies a modified product generally a toxin,
which is not able to interact with the product of the
allele for susceptibility in the host.

Resist
ance
gene
Virulence gene
Incompatibility Compatibility
A1 a1 A1 a1
R1 R S R R
r1 S S R S

• Which variety is the most susceptible and why?
• Which variety is the most resistant and why?
• Which variety is the most tolerant and why?
• Which variety is the most sensitive and why?
Variety Virus conc. Yellowing Yield with
virus (kg)
Yield without
virus (kg)
A 100 8 80 90
B 60 5 100 110
C 50 4 75 90
D 70 6 50 100

Question
With the help of following given
table write the genotypes of the
host (A, B and F1) and pathotype
and inheritance of resistance.

Patho
type
Variety Progeny ratio
A B F1 F2
P1 R S All R 3 R 1 S
P2 S R All R 3 R 1 S
P3 R R All R 15 R 1 S
P1+
P2
S S All R 9 R 7 S

Genotypes:
Var A: AAbb Var B: aaBB
F1: AaBb P1: A1A1a2a2
P2: a1a1A2A2 P3: A1a1A2a2
P1+P2: A1A1a2a2+a1a1A2A2

Inheritance of resistance
• Inoculum P1 or P2: F2 ratio, 3;1;
single gene with two alleles
• Inoculum P3: F2 ratio, 15: 1;
duplicate gene action
• Inoculum P1 + P2: F2 ratio, 9 : 7;
complementary gene action.

Types of resistance
• 1. Broad Resistance: Resistance that results from
an identifiable mechanism that is effective to
several species of potential NE.
Example: Toxic alkaloids in potato, glucosinolates
in Brassica, latex production in Asclepias.
▪ Active R: becomes operative in reaction to an
attempt of infection by NE. Eg, phytoalexins
(pisatin,phaseolin, nishitin, betagarin), PR- protins,
formation of papillae.
▪ Passive R: present already before the onset of the
infection process, and that is not the reaction to an
attempt to infection by NE. Eg, alkaloids in potato.

Non-host resistance
• The complex of characters of a plant species that
are responsible for making it a non-host to a
certain potential NE is non-host resistance. Plant
species of which no single individual is susceptible
to a NE is called as non-host.
• Host range: List of plant species that can be
exploited be a NE as source of nutrients.
• Generalists/polyphagous: NE with a wide host
range.
• Specialists/oligophagous/monophagous: NE with a
narrow host range or even a single plant species.

• Race: A group of genotypes within a pathogen species
that is distinguished by its virulence spectrum.
• Biotype: synonym of race but used for phytophagous
insects and nematodes and for parasitic higher plants.
(Virus and Bacteria: biotype; Nematode: pathotype
term is used in stead of the term race)
• Forma specialis: Unit within the natural enemy species
that is distinguished by its host range; differ in
pathogenicity (capacity of a microbial organism to
infect a plant species) but belong to the same
pathogen species.

Mechanisms of non-host Resistance
• May not be stimulated to germinate: soil borne
pathogen, nematode
• Spore germinate but fail to penetrate: leaf
pathogens
• Penetrate the epidermis cell and abort just before
or after the plant cell penetration
• Blocking of plant cell wall penetration by
formation of papillae
• Cell wall penetration and necrosis of plant cell

Breeding for non-host resistance
• Crossing between non-host and cultivated species
and selection of target plant generation after
generation
• Protoplast fusion of non-host and host plants and
grow regenerants then repeatedly backcrossing to
the host species

Hypersensitivity Resistance
• Hypersensitivity: Capacity of a plant to defend
itself against a pathogen/parasite by reacting with
necrosis of plant cells at the infection sites.
• Mechanism occurs as reaction to infection by
biotroph and hemibiotroph
• It is an active defence mechanism
• Associated with other active defence mechanisms
like production of phytoalexins and pathogen
related proteins
• Immune: showing no macroscopic visible sign of
infection whatsoever after exposure to a pathogen

• Virulent: Pathogen genotypes to which the
resistance is not effective.
• Avirulent: Pathogen genotypes to which
the resistance is effective.
• Isolate: A sample of pathogen/parasite,
that is stored alive or maintained in
isolation on plants or in nutrient media.

What levels of specialization by Septoria tritici can be discerned? What terms are
used for these levels of specialization?
Species Cultivars Isolates: Septoria
tritici
T. durum 1 2 3 4
A 44 43 0 1
B 40 42 18 20
C 02 20 0 1
T. aestivum 0 0 15 18

1. Do you find race specific and race non specific resistances? If so, which lines are
race specific and which are race non specific to which isolate(s)? 2. How would you
determine on how many genes the resistance of line A against isolate 1 is based? 3.
How would you determine whether the resistance of line E against isolate 1 is based
on the same gene as the resistance of line A against that isolate?
.
Breeding
line
Isolate of Bremia lactucae
1 2 3 4 5
A 0 0 0 0 0
B 20 0 22 19 19
C 10 9 13 10 9
D 51 53 55 54 52
E 0 0 35 23 23

• Race specific B and E
• Cross A x D and test F2 segregation for
resistance
• Cross E x D and test F2 segregation for
resistance
• Cross E x A and test F2 segregation for
resistance, if these cultivars have the
same resistance gene effective, no
segregation in F2 such as R1R1 x R1R1.

• With the help of following table, how many races of
Melampsora lini are represented at least by these 5
isolates? Is a gene for gene relationship likely?
Deduce how many different genes for resistance are
at least necessary to explain these results.
Cultivars Isolates of Melampsora lini
1 2 3 4 5
Pinto + + - + +
Remon - + - - +
Marco - - + + -
Vesuvius - + + - +
Clara - - - - -

Answer of 4.4.1.4
Cultivar Isolates
1
A1A1a2a2
a3a3
2
a1a1A2A2
a3a3
3
A1a1a2a2
A3A3
A
r1r1r2r2r3r3
+ + +
B
R1R1r2r2R3R3
- + -
C
r1r1R2R2R3R3
+ - -

• A X B A X C B X C
F1 F1 F1
F2 F2 F2
3R:1S 3R:1S ALL R

Expression of Resistance genes
• Resistance allele (incomplete, complete )
• Genetic background of cultivars
• Genotype of the pathogen like homozygous, heterozygous
state
• Developmental stage of the plant
• Environmental factors like temperature

Supressors
• Supressors are those that prevents the
expression of defence genes and stop the
resistance reaction
• They are either dominant or recessive.

• Two homozygous host plants are
intercrossed. Both have the same dominant
major gene for hypersensitivity resistance.
One of the two plants, however also has a
dominant gene for suppression of resistance.
The other plant has a recessive allele on the
suppressor locus that does not interfere with
the expression of resistance. In what
frequencies do you expect resistant and
susceptible phenotypes in the two parents,
F1 and F2 after inoculation with a pathogen
isolate carrying the corresponding allele for
avirulence?

• R1R1, SS X R1R1, ss
Sus. Res.
• F1 R1R1, Ss (Sus.)
• F2 1R1R1, SS : 2R1R1, Ss : 1R1R1, ss
Sus. Sus. Res.

Nomenclature of R genes
• On the basis of name of disease( Yr genes:
yellow rust of wheat caused by Puccinia
striformis), scientific or English name of
pathogen (Cf genes in tomato against
Cladosporium fulvum), resistance reaction (R
genes in potato against Phytophthora infestans)
• Resistant genes are either dominant or
recessive. Dominant genes are indicated by
capital letter.

Nomenclature of Race
• Mostly based on the genes for resistance that are ineffective
to the race. Eg, Race(1,3) is virulent on cultivars with the
genes R1 and or R3.
• Based on the genes for resistance that are
ineffective/effective to the race. Eg, Leaf rust caused by P.
hordei. Race(1,2,4,5,6,8/3,7,9) is virulent on barley cultivars
with the genes Pa-1,2,4,5,6,8 and avirulent with the genes Pa-
3,7,9.

Answer 4.4.1.8
• Race indication for A to D
• A: 2,3,4 / 1
• B: 1,2 / 3,4
• C: 2,3 / 1,4
• D: 0 / 1,2,3,4
• Differential set of 3 lines distinguished by 8 races
Cv 1 2 3 4 5 6 7 8
A + + + + - - - -
B + + - - + + - -
C + - + - + - + -

Differential Set
• A set of lines or cultivars by which races of a
natural enemy can be characterized or
distinguished.
• To determine the virulence spectrum of isolates,
differential set of cultivars is used.
• Differential interaction is a phenomenon that
the ranking in susceptibility of two plant
genotypes depends on the genotypes of the
pathogen isolates to which they are exposed.
There is a clear cultivar x race interaction.

How many races can be discerned maximally by a
differential set of cultivars consisting of only 5
lines? (2n, n = no. of lines)
Flax Cultivars Isolates of Melampsora lini
1 2 3 4 5
Pinto + + - + +
Remon - + - - +
Marco - - + + -
Vesuvius - + + - +
Clara - - - - -
Differential interaction

Durability
• Breaking down of resistance: Phenomenon that
the effectiveness of resistance against a natural
enemy decreases as a result of changes in the
population of that enemy.
• Durable resistance: Resistance that remain
effective for a long period in which it is applied
at large scale in an environment conducive to the
natural enemy.
• Within the same plant-patho system, the degree
of durability of the resistance varies.

• Hypersensitivity resistance is infamous
for its very limited durability.
• Hypersensitivity against PM, DM, rust
fungi and loose smut are usually very
ephemeral.
• These pathogens are all biotroph or
hemibiotroph with a narrow host range
and a large number of races known.

Causes of Breaking down of resistance
• Primarily the consequence of a loss mutation in
the avirulence locus in the pathogen. AVR 1 to
avr1.
• Immigration
• Recombination: AVR1avr2 x avr1AVR2 gives 15
avirulent : 1 virulent (i.e., avr1avr2) genotypes of
pathogen.

Partial resistance
• Resistance that results in a reduced epidemic built-up of the
natural enemy, despite a susceptible, non hypersensitivity
infection type.
• Applied with biotroph, hemi biotroph plant-patho systems.
• Many crops to PM and rust, in potato to phytophthora
infestans and in rice to Xanthomonas oryzae and Pyricularia
oryzae.

Components of Partial Resistance
• Latency Period: Time between the onset of
the infection process and the reproduction of
the pathogen.
• Infection frequency: Percentage of spores
that result in a reproducing infection but also
for the number of infections observed per
plant, per leaf or per cm2 tissue.
• Spore production per uredosorus (barley leaf
rust)

• Per plant-patho system the components that
constitute the partial resistance may differ.
For eg, partial resistance in rice against P. oryzae
is not due to a prolonged latency period, but
mainly due to a reduction of the infection
frequency and a lower rate of lesion growth.
• The level of partial resistance can only be
determined directly in polycyclic field
experiments.

• Monocyclic :
1. (natural enemy) In one growing season
completely only one sexual/asexual reproduction
cycle.
2. (test) with evaluations being carried out during
one reproduction cycle of the natural enemy.
• Polycyclic:
1. (natural enemy) Having several sexual/asexual
reproduction cycles per crop growing season.
2. (test) with evaluations carried out after several
reproduction cycles of the natural enemy.

Partial resistance of host genotype depends on:
• Degree of correlation of the component with the
PR
• Experimental error
• Convenience and ease of measurement of the
components
• Degree of correlation between the individual
components

Mechanisms of PR
• A certain crop architecture may result in lower air humidity
in the crop, or in a lower deposition of spores and such
effects may lead as with partial resistance.
• Plant cell wall penetration, growth and reproduction of the
pathogen are less successful than on a more susceptible
plants.
• Partial resistance is associated with the formation of
papillae.
• Many pathogens infect young plants and young plant tissue
more effectively than older plants and plant tissues.
• The latency period tends to be shorter on seedlings than on
older plants, and on young leaves shorter than on the older
leaves.

Genetics of partial resistance
• In general, partial resistance is a quantitative trait.
• Partial resistance is governed by many genes,
polygenes, combination of additive genes that
each have a small effect.
• When progeny of a cross between parents with a
different level of partial resistance are tested, a
quantitative continuous segregation is found.
• Transgressive segregants is found.
• Concluded that both parents carry genes for partial
resistance at different QTLs.
• Monogenic gene: ml-0 of barley to PM and Lr34 of
wheat to leaf rust.

Hypothetical example: Tannin concentration
• Host: R1 and R2 Pathogen AVR1 and AVR2
• R1R1 = 10, R2R2= 5 A1A1 = 5 and A2A2 = 15
• Susceptible plant: 25 (due to other genes)
Host Gen Pathogen genotypes
a1a1a2a2 A1A1a2a2 a1a1A2A2 A1A1A2A2
r1r1r2r2 25 20 10 5
R1R1r2r2 35 30 20 15
r1r1R2R2 30 25 15 10
R1R1R2R2 40 35 25 20

Residual resistance
• When the hypersensitivity resistance is
completely expressed, the effect of the
genes for PR may not be seen directly, since
the plant is completely resistant.
• A new virulent race appears, the plant will
be affected.
• Extent of infection is depends on the level
of PR in the genetic background of that
plant.

• Durable resistance: Resistance that remain
effective for a long period in which it is
applied at large scale in an environment
conducive to the natural enemy.
• Residual resistance: The resistance that
may be observed after a virulent race of
the pathogen appears and infects a
formerly completely resistant cultivar is a
residual resistance.

With the help of following given results, which cultivar
has the highest level of partial resistance? Give your
logics.
Components of
Partial Resistance
Cultivars
A B C D
Infection frequency
(%) 100 75 40 60
Latency period
(days) 8 10 15 17
Spore production/
Uredospore (No.) 100 65 50 90

• On the basis of following information, which
cultivar is durable over a long period for the
concerned pathogen and why?
Cultivars Cultivars’ genotypes Pathogens’genotypes
A R1R1R2R2 AV1AV1AV2AV2
B R1R1R2R2R3R3 AV1AV1AV2AV2AV3av3
C R1R1R2R2R3R3R4R4 AV1AV1AV2AV2AV3AV3AV4av4
D R1R1R2R2R3R3R4R4R5R5
AV1AV1AV2AV2AV3av3AV4AV4AV5AV5
E R1R1R2R2R3R3R4R4R5R5R6R6
AV1AV1AV2AV2AV3av3AV4av4AV5AV5AV6av6

Types of natural enemy and defence
mechanisms
• Vertebrates: broad resistance, avoidance, non-
preference
• Insects and lower animals: broad resistance,
hypersensitivity resistance, avoidance, genetic
modification, escape, non-preference
• Nematodes: hypersensitivity resistance, tolerance,
escape
• Parasitic plants: resistance and tolerance
• Biotroph/Hemi-biotroph fungi: hypersensitivity and
partial resistance
• Necrotroph fungi: Partial resistance(monogenic and
or polygenic)

Types of natural enemy and defence mechanisms
Contd..
• Vascular wilts: tolerance, resistance
• Weakness parasites: resistance,
avoidance
• Bacteria: resistance
• Phytoplasms and rickettsia’s: resistance
• Viruses: resistance, tolerance
• Viroids: resistance, tolerance

Consideration in the introduction of
resistance
• Epidemics or plagues of natural enemy
• Economic damage caused by natural enemy
• Control of natural enemy by other means
• Investment
• Earning back of investment
• Risky!

Sources of resistance
• The cultivar itself: allogamous crops than autogamous
crops
• Commercial cultivars
• Other varieties
• Landraces
• Wild progenitor species: same botanical species
• Related species
• Related genera
• Non host
• Mutations
• Somaclonal variation
• Unrelated organisms
• Germplasm collection

Why landraces, wild progenitor,
related species and genera?
•Adaptation
•Quality
•Disease
•Insects
•Yield

Drawbacks of wild progenitor, related species and
genera
• Limited crossability
• Hybrid sterility
• Poor chromosome pairing and poor
exchange of chromosome fragments
• Lower fertility
• Frequent backcrossing and selection to
get rid of the numerous undesirable
traits of the donor

Alternative methods of creating
resistance
• Induction of mutation
• Genetic modification
• Pathogen specific genes from plants
• Genes for broad resistance
• Non vegetable genes (Bt gene)
• Genes of viral origin (coat protein)

Considerations of mutagenic treatment
• Not necessarily durable
• Low frequency of the mutation for
resistance
• Huge number of plants should be
tested
• Efficient methods of screening
• Undesirable side effects

Disadvantages of genetic modification of crop
plants
• Recalcitrant to genetic
transformation (monocotyledons,
leguminosae)
• Public acceptance is low
• Genes are not always expressed
• Breaking down of resistance

Tests of plants
Field test
• Simple and not expensive
• Environmental conditions are not controlled
• Growing conditions are quite representative for
commercial cultivation
• Once in a growing season
• Natural enemy distributed heterogeneously
• Escape of infection
• Occurrence of other biotic and abiotic factors
• Polycyclic (PM, rusts, P. infestans)

Greenhouse test
• Controlled environmental conditions
• Applied with seedlings or young plants
• Growing conditions are not quite representative for
commercial cultivation
• Natural enemy distributed homogeneously
• Escape of infection is low and evaluation relatively
simple
• Chance of occurrence of other biotic and abiotic
factors is low
• Monocyclic
• Plants tend to appear more susceptible than in the
field

Laboratory test
• Tests are performed on germinating seeds, leaf
disks, detached leaves or in vitro cultures
• Advantages/disadvantages are as with
greenhouse tests, but pronounced

Stage of developments to be tested
Advantages of seedling test over mature plants
• Require less space
• Performed soon after sowing
• Inoculated more uniformly
• Uniform in developmental stage

Disadvantages of seedlings test
• Numerous genes for hypersensitivity that are
only effective in mature plants
• Partial resistance against rust and PM fungi is
usually less pronounced in seedlings than in
later stage of plant development
• Natural enemies specialized to live on fruits,
flowers or stems is escaped to test

How to apply natural enemy?
• Dipping: soil borne pathogen; seeds or roots
of the seedlings
• Spraying: leaf pathogen (PM, P. infestans, rust
fungi, Septoria tritici)
• Dusting: leaf pathogen (PM, P. infestans, rust
fungi, Septoria tritici)
• Injection: Xanthomonas campestris pv oryzae
• Disadvantage of injection: avoidance and
resistance!

Using spreader plant
• A susceptible cultivar is planted in a
row behind the test plots and
perpendicular to the plant rows in
the plots.
• The spreader rows are inoculated
early in the season.

How to compose the inoculum?
Aspects to be considered
• Phytosanitary aspects: no exotic races can be
used
• Screen and characterize the pathogen by using
differential set of cultivars or by molecular
marker fingerprints
• Known variation in the pathogen
• most naturally occurring complex race

Composition of inoculum
• A single isolate
• Mixture of isolates

Mixture of Isolates
• Test will be carried out with the
most complex race (race with a wide
virulence spectrum) available
• Mixture of isolates belonging to
various races that have as many as
virulence factors represented

Question
• Suppose that in a plant pathosystem 8 race specific genes for
resistance are known to occur, R1 to R8. In the pathogen many
races are known that are virulent for one or more of these
resistance genes. New resistance is looked for in material
received from a germplasm collection. Of course such resistance
will only be worth while, when the pathogen population has no
corresponding virulence to the new resistance gene.
• There is no super complex race available that combines virulence
to all 8 resistance genes. There are isolates belonging to the
races 1.2.3.4., 1.5.6. and 2.7.8. These isolates are mixed and the
germplasm is inoculated with the mixture . Some accessions in
the collection are completely resistant to this mixture.
Give your logical explanation.

Answer
• Unbroken gene for resistance; pathogen
has may be not yet the corresponding
AVR gene.
• Some accessions have a combination of
known resistance genes like R3 and R8,
R2 and R6, R4 and R7, R4 and R5, etc.

Interpret the following results
Tested
cultiva
rs
Infected
lesions caused
by mixtures
Result I Result II
Isolate 1 to 4 Isolate Isolate
1 2 3 4 1 2 3 4
A 160 40 40 40 40 40 40 40 40
B 60 15 15 15 15 20 0 20 20
C 40 10 10 10 10 20 20 0 0

• In Result I could be race non specific. Resistance is
equally effective to all isolates. Cultivar A and D are
relatively susceptible and resistant respectively.
Resistance is equally effective to all isolates.
• In Result II, cultivar A is race non specific but
cultivar B, C and D are race specific. Cultivar B is
resistant to isolate 2, C is resistant to isolate 3 and 4
and D is resistant to isolate 1, 2 and 3. Resistance is
not equally effective to all isolates except cultivar A.
• Partial, race non specific resistance should be
looked for with genetically pure isolates rather than
with mixtures

Incubation
Factors
• Relative air humidity
• Temperature
• Light intensity
Such conditions can be controlled much better in
the labs and greenhouse than in the field.

What aspects to evaluate?
• After incubation the effects of the infection
may become visible
• Show symptoms or biting damage
• Differ in degree or nature of infection or
severity of symptoms expression
• Strong indications of differences in resistance
• Relatively mild symptoms may also indicate
tolerance

Quantitative aspects
• Incidence: degree of infection in a population of
the host species that is expressed as the
percentage infected or symptoms showing
individuals
• Polycyclic leaf pathogens: percentage of leaf
tissue covered with lesions, mycelium or
postules
• AUDPC: amount of infection
• Measurement: Visual, image analysis,
biochemical or serological tests
• Lower the AUDPC value, considered as resistant
cultivar

• AUDPC = Sum of (X1 + X2)/2 X
(T2-T1) + (X2 + X3)/2 X (T3 –T2)
+……………..+(Xm + Xn)/2 X (Tn -
Tm). Whereas X1, X2 , .....Xm, Xn
are the disease severity on the
respective date and T1 ,T2 ,
.....Tm, Tn are the dates on which
the disease is scored.

Measurement
(Helminthosporium )
•Single Digit System
•Double Digit System

Single Digit Double Digit
Scoring individual tiller
basis
Scoring per plot basis
Difficult/Tedious Easy to perform
Accurate Inaccurate
Experiment having few
research plots
Experiment having many
research plots
Genotypes evaluated
rather quickly
Genotypes evaluated
quickly
Practiced whether time is
not a limiting factor
Practiced whether time is a
limiting factor

• First Digit (D1): Relative height upto
where the disease is appeared. E.g., 1:
bottom of plant, 9: top of plant.
• Second Digit (D2): Relative severity of
the disease. How severely the plants
are affected by the concerned disease?
• % Severity = (D1/9 x D2/9) x 100%

Score Leaves No.
1 1,2
2 3
3 3,4
4 4,5
5 5,6,7
6 7,8
7 8,9
8 9
9 Spike

Calculate AUDPC based on following information and determine
which genotype is most resistant (Date of interval 7 days)
CULTIV
ARS
DATE 1 DATE 2 DATE 3
D1 D2 D1 D2 D1 D2
A 1 1 3 3 5 4
B 0 0 2 1 3 3
C 3 2 4 4 6 5
D 3 3 6 5 7 6
E 4 3 7 6 8 7

Calculate AUDPC based on following information and determine which
genotype is most resistant.

Components of resistance
• Latency period
• Infection frequency
• Number of spores produced per fruiting
body

Assessment of damage
• Reduction of physical or economic yield is
damage
• Higher the amount of infection, the higher
damage should be expected
• Quantity of the pathogen relative to that on a
susceptible cultivar is determined by the
level of resistance or avoidance
• Amount of damage is determined by both
the amount of pathogen and the level of
tolerance

• Heterogeneity of soil fertility cause a
large experimental error
• Perform in replicated trials
• Cultivars with the least yield reduction
are of course the most desirable
• Can either be resistant or tolerant or
combination of both

How to determine?
• Resistance: amount of pathogen in or on
cultivar
• Tolerance:
• Yield/value of cultivars in the absence of
pathogen
• Yield/value of cultivars in exposed conditions
of pathogen
• Per unit of pathogen in order to calculate the
damage

• Sensitivity = { (Yield without
pathogen -Yield with pathogen)/
Yield without pathogen}/ Con. of
the pathogen
• Higher the sensitivity, the higher
the damage

Effect of PM on yield reduction of 6 barley
cultivars with different levels of tolerance and
or resistance is given below. With the help of
that given information, interpret it.
Cultivar Infection
(%leaf area)
% yield reduction
Observed Due to
Lack of Res Lack of Tol
A 80 21 21 0
B 60 18.5 15 3.5
C 50 12 12 0
D 50 7 12 -5
E 40 12.5 9 3.5
F 20 3 3 0

Interpretation
• Higher the figure the more susceptible or
sensitive the cultivar
• Negative values indicate tolerance or resistance
• The most tolerant cultivar is D, Why?
• The most resistance cultivar is F, Why?
• The most sensitive cultivar is B and E, Why?
• The most susceptible cultivar is A, Why?

• A scientist carries out a screening for
tolerance with regard to damage by
PM in several cultivars. He used one
infection free yield trial by applying
pesticides and the other infected.
What is the purpose of the infection
free yield trial? Suppose the fungicide
used is quite phytotoxic, How does this
affect the assessment of the level of
tolerance?

• To determine the yield reduction.
Difference in yield between infection
free and infected trials gives the
damage.
• If phytotoxic, it will decrease the yield
of the infection free trial. Difference
between the infection free and
infected trials will be underestimated
and the tolerance will be
overestimated.

Suppose:
• Yield w/o pathogen, w/o phytotoxic: 10
t/ha
• Yield w/o pathogen with phytotoxic: 9.5
t/ha
• Yield w/ pathogen: 8 t/ha
• Real yield loss: 2 t/ha
• Apparent yield loss: 1.5 t/ha
• Therefore the real damage will be under
estimated and the tolerance will be over
estimated.

Qualitative aspects
• Infection type actually indicates the intensity of
the hypersensitivity reaction
• Amount of necrosis and chlorosis at the
infection site, and the rate of sporulation of the
individual colonies are to be considered.
• Rust, blast and blights
• Mixture of reactions within the same plant,
depending on dev. stage, age and quality of leaf
• Infection classes: R, MR, MS and S

Breeding material of a cereal crop and infection by
PM/rust fungi is given below.
What is the meaning of letters and figures and aspects of the
infection?
Line Infection
type
Line Infection
type
1 45S 6 5MR
2 20S 7 50R
3 0R 8 5S
4 20MS 9 10MR
5 80S 10 5MR

• Which line(s) do you select for
breeding program? And why?
• Which line is the most resistant,
tolerant and susceptible?

• Which of the 10 lines (given in slide
no. 84)are especially interesting to
include in a breeding program for
resistance ?
• Line 8: Partial resistance, durable
type of resistance
• Line 3: Resistant, but non durable!

Factors governing over or
under estimating the resistance
• Differences in earliness between
accessions
• Inter plot interference
• Inoculum dose
• Moment of evaluation

Differences in earliness
• Lines will differ from each other in earliness
• Due to development rate
• Early genotype (flag leaf) exposed longer to the
pathogen than late genotype and tends to look
more susceptible, Potato: P. infestans
• Early plants will escape from heavy infection by
NE that appear late in the season, late cultivars
may escape or recover from infection by NE that
thrive earlier in the season (Isreal cereal: PM
earlier in the season, Septoria later in the season)
• Early lines should be compared with early checks
and late lines with late checks

Inter plot interference
• Phenomenon that in an experimental field with
small adjacent plots plant genotypes with
quantitative resistance are infected more
severely, and susceptible plants less severely
than when they would be grown in isolated field.

• With polycyclic air borne pathogens the resistant lines
will receive a large amount of inoculum from its
susceptible neighbour, while it hardly exports inoculum.
• Infection level of the resistant lines will be much higher
than would have been the case in a monoculture of that
plant genotype.
• Susceptible lines have a much larger export than import
of spores.
• Susceptible lines will consequently have a lower level of
infection than they would have had in monoculture
situation.
• Results shows over and underestimation of the
differences in resistance level.
• This phenomenon is inter plot interference.

How to minimize the effects of Inter plot interference?
• Plots/plant rows can be alternated with rows
of a fast growing and rather tall non host crop
• Evaluate only the inner plants rows of multi
row plots
• A possible spreader row close to the plots
should be grown to avoid escape. Then cut
away the spreader row once the pathogen has
established itself in the experimental field.

Test of inter plot interference
• The lines that are to be tested is grown in
experimental plots along with susceptible line.
• These lines is to be grown in monoculture
situation.
• Record the level of infection in both situations
• Estimate the difference

Example of Inter plot interference
Date Cultivar
Barley
Isolat
ed Plot
Inter plot
4.5 x 4 4.5 x
4.5
4.5 x
1.5
4.5 x
0.25
21 / 6 Vada 15 1000 1600 4500
10 / 7 Akka 18000 20000 22000 18000
TIMES 1200 20 14 4

Amount of inoculum
• Over and under estimation of resistance
occurs when too high or too low doses of
inoculum are applied at plants.
• A low doses of inoculum of, for eg., a soil
borne pathogen in the field may result in a
high frequency of escape. Plants that are
susceptible escape from infection qualified as
resistant!
• Too high doses of inoculum may obscure
quantitative differences in resistance.

Moment of evaluation
• Especially relevant for partial resistance.
• Possible differences in amount of
infection may depend on the moment of
evaluation.
• In greenhouse, monocyclic tests are
performed.
• Moment of assessment is very important
for like latency period of a rest disease in
cereal.

• In greenhouse if observation is made too early
for mature postules, none of the lines show
infection. If too late, all lines carry mature
postules. This is the apparent differences in
latency period.
• Too early and too late an assessment may
result in a serious over and under estimation of
resistance.
• In field, polycyclic tests are performed.
• Early in polycyclic field test, differences in
amount of infection are hard to judge because
of low over all level of infection.

• Epidemic progresses the differences between
lines increases.
• Later in the season, most susceptible lines
are completely infected by the pathogen.
• At this moment the differences between lines
are greatest.
• From then on, the difference will decrease
and slightly and fairly resistant lines may also
become completely infected in the end.
• Too early and too late an assessment may
result in a serious over and under estimation
of resistance.

What type of plant defence to select?
• Avoidance
• Non-preference: if many genotypes are
grown, if grown in monoculture: accept
Impression of the breeder!!!
• Non-acceptance: monoculture
• Tolerance (difficult to judge whether the
difference is due to Resistance or
tolerance)

•Broad resistance
Effective for several natural enemies.
Side effects: food and fodder crops;
quality of the crop and harvested
product may be affected; level of
toxicity increases, increased
attractiveness to specialists species

Hypersensitivity resistance
▪ Cultivar protected completely from
infection
▪ Inherits monogenically
▪ High heritability
▪ Most applicable to race specific pathogen
▪ Breaking down of resistance occurs
▪ Apply gene pyramiding, diversification
and cultivar mixture strategies

Partial resistance
▪ Recognition is not straight forward
▪ Polygenic inheritance
▪ Applied mainly in field crops and
fodder crops
▪ Reduce the number of pesticide
treatments
▪ Quite durable than hypersensitivity
resistance

What type of plant defence to select?
A summary
▪ Hypersensitivity resistance is the best option in
a number of plant patho systems
▪ Partial resistance is best option if breaking down
of resistance occurs
▪ Avoidance, non preference and non preference
mechanisms are best options for insects
▪ Broad resistance is applicable to generalists
▪ Race specific hypersensitivity resistance may be
applied in well conceived strategies by gene
pyramiding, diversification and cultivar mixtures
▪ Breeding for tolerance is too labourious

Selection procedure
Earlier stage of breeding process: qualitative
traits and in advanced stage quantitative
traits, eg, yield.
Early stage of breeding process
➢Many accessions, few individuals/accession
➢When the resistance
▪ Behaves as qualitative trait
▪ Occurs in low frequency in the starting
germplasm
▪ Is indispensable for a successful commercial
cultivar
▪ Can be judged in a simple, cheap and rapid test

Selection procedure
Backcrossing
• Applicable to hypersensitivity resistance
• Generally in autogamous crops
• Select donor and recipient parents
• Cross them
• Back cross and repeated back crossing to
susceptible recurrent parent to eliminate the
undesirable genes of donor
• Select resistant progeny per generation
• Use molecular markers to improve the efficiency
of the back cross procedure
• Go up to BC6 to BC8 generation

Selection procedure
Recurrent selection
• Applicable to partial resistance
• Inheritance is quantitative or polygenic
• Applicable in both allogamous and
autogamous crops.
• When major genes for hypersensitivity are
present aimed at partial resistance, it is often
recommended to discard not only the
extremely susceptible but also the
completely resistant plants.

Vertifolia effect
• Presumed loss of genes for residual resistance
by random drift during the crossing and
selection process, caused by the fact that genes
for complete resistance mask the effects of
possible quantitative resistance in the genetic
background.
• Refers to an epidemic development in a variety
carrying vertical resistance genes and a low
level of horizontal resistance leading to heavy
economic losses.

Why Boom and Bust Cycle?
• Genetic system of the pathogen
• Selection pressure exerted by
the host on the pathogen
pathotypes

Boom and Bust cycle
• When a new variety carrying VR is developed, it is
resistant to the prevalent pathotypes of the pathogen and
becomes popular rapidly and occupies a large proportion
of the growing areas under the concerned crop. This
period of Boom continues till the pathotype specific to the
VR gen(s) employed in the variety evolves and/or
increases in frequency to cause an epidemic in the fields
occupied by the variety.
• The now susceptible variety loses popularity and area
under it declines sharply thus the variety is effectively
busted by the virulent pathotype. This is called boom and
bust cycle.
• When a variety goes bust, breeders develop a new variety
with a new VR gene, which makes it resistant to the
predominant pathotype. This variety also under goes the
boom and bust cycle.

• Boom and bust cycle lies in the genetic system of
the pathogen and the selection pressure exerted by
the host on the pathogen pathotypes.
• When a resistant variety becomes popular, it is
cultivated on large areas. This will increase the
selection pressure in favour of the pathotype
virulent on the variety; as a result, the frequency of
this pathotype in the pathogen population will
increase.
• The popularity of and the area under the variety will
decline rapidly following the epidemic. This will
reduce or eliminate the selection pressure in favour
of the pathotype virulent on the variety; as a result,
the frequency of this pathotype in the pathogen
population will also decline.

Use of molecular markers
• Monogenically controlled hypersensitivity
resistance and quantitatively inherited
inheritance
• Close linkage of markers and genes
• Replacement of direct selection by indirect
selection

Advantages of using molecular markers
• Race specific resistance may be distinguished
• Useful in pyramiding genes for resistance
• Used to visualize the loci for quantitative
resistance
• Compilation of QTLs from different donors
into one genotype in order to raise the level
of quantitative resistance
• Making backcrossing procedures much more
efficient

Non durable resistance
Why?
• Hypersensitivity resistance is non durable in
general
• Pathogen population becomes
predominantly virulent, when one gene after
the other is introduced
• All genes for resistance available in the crop
will be finished

Strategies to enhance the durability
• To hamper the formation of virulent
race
• To hamper the permanent
establishment, reproduction and
dispersion of such a virulent race

Strategies for controlling plant
pathogens and pests
• Exclusion of pathogen from the host: (legislation,
plant quarantine, crop inspection or crop isolation)
• Reduction or elimination of the pathogen’s
inoculum (crop rotation, sanitation, soil drainage,
weeding, soil sterilization, seed treatment
• Improvement of host resistance: introduction of
genetic resistance into adapted cultivars
• Protection of the host by using chemicals
(pesticides)

Applications of non durable resistance
1. Pyramiding of resistance genes: The pathogen would
need a double or multiple mutation to breakdown
the resistance in that cultivar. It ultimately hampers
the formation of a virulent race.
Conditions
▪ Pathogen should be uniformly avirulent to the
resistance gene, the allele frequency of the
corresponding Avr genes should be 1.
▪ Combined genes for resistance should not overlapped
in several cultivars
▪ Cultivars may not be grown in which the resistance
gene occurs separately

Interpret the result based on following given information about type of
resistance and durability
Crop Variety Pathogen Durability
of Variety
wheat A Pa 3 Y
B Pb 5 Y
C Pc 15 Y
D Pd 40 Y
Potato X Px 2
Y Py 10
Z Pz 10

Ways to distinguish progeny carrying parental resistance
genes in combination
• Races that are virulent to either of the
resistance gene may be applied
• By test cross: F2 progeny15 R: 1S (with two R
genes); 3R : 1S (with one R genes)
• Hybrid: by providing parental inbred lines
with different resistance genes
• By the use of markers: Progeny carrying
resistance genes can be identified indirectly
by their marker phenotype

2. Diversification:
▪ Mixtures of genotypes carrying various genes for resistance
▪ Each plant genotype will be susceptible to at most a fraction
of pathogen population
▪ The pathogen is submitted to a varying selection pressure
because of the diversity in resistance gene.

3. Use of Multilines
▪ Multiline is a cultivar consists of a mixture of near
isogenic lines that differ only in their genes for
resistance to a certain natural enemy species.
▪ Predominantly applicable to autogamous crops
▪ Stabilizing selection: Phenomenon that in a
pathogen species the frequency of virulence and
avirulence genes is determined both by the
frequency and effect of the corresponding
resistance genes in the host population and by the
difference in fitness between a virulent and
avirulent isolate on a susceptible host plant.
▪ It is of two types: Dirty and Clean multilines

• Avirulence gene plays a important role in the
physiological functions in the pathogen.
• A deletion of the avirulence gene should result
in a decreased fitness of the pathogen.
• An attractive idea!
• Principle of stabilizing selection is introduced
by Vanderplank, a South African
epidemiologist.
• Selective advantage of a complex race would
be an offset to the disadvantage of a reduced
fitness.

Contradiction to the stabilizing selection
principle
• Complex races are viable.
• No large and consistent difference in fitness
between virulent and avirulent isolates is
detected.
• There is a discrepancy between the frequency of
virulence genes in the pathogen and the
frequency of resistance genes in the host.

Fitness of pathogen: Examples
• Tomato: Cf9 gene: avr9 appears now
and then. AVR9 gene plays a role in the
fitness of the pathogen
• Tomato/Tobacco: (TMV): gene Tm22 in
host. avr Tm22 identified in lab test. In
commercial cultivation such virulent
strain has hardly or never been found.

4. Cultivar Mixtures
• Cultivar mixtures consist of various cultivars
that have different genes for resistance.
• Selected from the diversification schemes in
list of recommended cultivars.
• Mixtures are of course not near isogenic lines
but are similar in features like plant height,
earliness.
• Because of agronomic heterogeneity,
acceptable for animal feed.

Question
• Why is not it feasible to realize a multiline
cultivar of potato with resistance to
Phytophthora infestans? What about a
cultivar mixture?
• Is it feasible to realize a multiline cultivar
of wheat with resistance to rust? What
about a cultivar mixture?

5. Integrated control
(a) Exploitation of the period without crop
▪ Many natural enemies pass a bottle neck at least
once a year
▪ Population increases in favourable periods and
decreases in unfavourable periods (host crop
unavailable)
▪ Genetic composition of the pathogen depends
largely on the genotypes surviving in the bottle
neck period
▪ Eg., Powdery mildew in barley. Virulent mutant
formed in summer will relatively survive less in
winter if winter barley is prohibited to grow.

(b) Crop rotation and phytosanitation
▪ Cultivation of different non host crop leads to a
decrease of the population of the pathogen by a
factor 2/3rd per year as compared to cultivation of
resistant cultivar by a factor 1/5th per year.
▪ Effective to soil borne pathogen and nematodes.
▪ Volunteer plants should be removed during the
season where other crop plants are grown.
▪ Strict inspections during production and trade of
sowing seed and propagating material serve to
eradicate infections at an early stage.
▪ Limit the size of pathogen population and chance
of virulent mutants to appear.

(c) Combination of resistance with biological
control
▪ Introduction of Tritrophic system
Three organisms/species (plant/host, pest and
predator of that pest) that mutually affect and
depend on each other.
▪ Growing completely resistant cultivar affects in
sustaining the predator species.
▪ Using toxic compounds may result decrease in
predator population indirectly.
▪ Balance in the tritrophic system is to be
maintained.

Breeding Methods: Disease Resistance
▪ Selection
▪ Introduction
▪ Hybridisation (pedigree and back cross)
▪ Mutation
▪ Somaclonal variation
▪ Genetic engineering

Factors affecting expression of disease and insect
resistance
• Certain specific factors may complicate breeding
for resistance that may be environmental or
biological in nature.
1. Environmental factors
• Temperature: Low or high temperature over a
period of time may cause loss of resistance.
• Light: Light intensity affects the chemical
composition of plants that is related to pest
resistance (e.g., glycoside in potato).
• Soil fertility: High soil fertility makes plants more
succulent and more susceptible to disease
development.

2. Biological factors
• Age: The response of a plant to a pathogen or
insect pest may vary with age. Some diseases
are more intense at the early stage in plant
growth than others.
• New pathotypes or biotypes: New variants of
the parasite that overcome the current
resistance in the host may exhibit a different
kind of disease expression.

Breeding for resistance to insects
Mechanisms
• Non preference: Character of a phytophagous species to
refuse (or accept less) a plant as a source of nutrients, when in
the environment more attractive alternatives are available.
• Non acceptance: Character of a phytophagous species to
refuse (or accept less) a plant as a source of nutrients,
irrespective whether or not in the environment attractive
alternatives are available.
• Antibiosis (Resistance): Refers to an adverse effect of feeding
on a host plant on the development and or reproduction of
the insect pest. In several cases, it may even lead to the death
of the insect pest.
• Tolerance (similar to disease tolerance)
• Avoidance: same as disease escape. It is not a case of true
insect resistance.

Nature of insect resistance
• Morphological features: hairiness, colour,
thickness, toughness, longer pedicels, devoid of
nector gland
• Physiological features: osmotic concentration of
cell sap, various exudates
• Biochemical factors: high concentration of
gossypol, benzyl alcohol, ethanol, soluble
compounds, 2-TD, saponin content

Sources of insect resistance
• The cultivated cultivar
• Commercial cultivars
• Other varieties
• Landraces
• Related species
• Related genera
• Unrelated organisms
• Germplasm collection

Screening techniques
i) field screening
ii) glass house screening

Durability of insect resistance
The appearance of new resistance breaking biotypes is
influenced by a variety of factors and they are as,
• Insect species
• Mode of inheritance of resistance: durability of
resistance is a function of number of genes present on
a crop species.
• Morphological characters and or anatomical
characters: hairiness, colour, thickness, toughness
• Biochemical factors

Breeding methods of insect resistance
i) Introduction
ii) Selection
iii) Hybridization: Pedigree method, Back
cross method
iv) Genetic engineering

GM strategies for insect resistance
• Use of bacterial insecticidal genes to provide
protection from pest damage: cry genes from
Bacillus thuringiensis. Cry proteins bind to
specific receptors in the insect larva midgut
causing selective pores in the midgut membrane
to open.
• Potential for using endogenous plant protection
mechanisms (copy nature approach)

Problem of insect resistance
to Bt:
• The specificity of Bt protein
receptor binding provides a
mechanism for the
development of insect
resistance to Bt.

Low levels of expression of
Cry genes
• Premature termination of transcription
• Splicing of Cry gene mRNA
• mRNA instability elements: AUUUA,
(ATTTA in DNA) determine the mRNA
instability in higher eukaryotes
• Biased codon usage

The Copy Nature Strategy
It is the alternative philosophy to the Bt magic bullet
approach. This strategy involves a rational approach to
the development of pest resistant crops and is
characterized by the following steps.
• Identification of leads: literature, world seed collection
• Protein purification: purification of crop proteins with
insecticidal properties, biosynthetic pathway would need
to be determined
• Artificial diet bioassay: determine the activity of isolated
protein against the target insect pests by performing
feeding assays in the laboratory
• Mammalian toxicity testing: toxicity of the protein
against mammals should be tested
• Genetic engineering: isolated gene transferred to the
crop plant

• Selection and testing: after transformation, selection of
transgenic plants, confirmation of transformation, inheritance
of transgene to the progeny and testing of expression levels
need to be carried out
• Biosafety: the effect of transgene to the crop yield, insect
damage, and the wider ecosystem should be properly
evaluated in the field trials
The aim of Copy Nature strategy has been stated as "insect
pest control which is relatively sustainable and
environmentally friendly". The strategy also takes account of
the fact that host plant resistance to pests is universal and
falls into two major categories.
• Horizontal resistance: Polygenic, cumulative effect of several
minor genes, does not involve gene-gene matching, durable
resistance
• Vertical resistance: Oligogenic, one major gene with high level
of expression, involve gene-gene matching, non durable

Strategies for countering the build up of
insect resistance
• Pyramiding more than one resistance genes in a transgenic
crop: cry2Ab and cry1Ac: cotton boll worm, beet army worm.
Cry1Fa and cry1Ac: Lepidoptera and coleopteran pests in
maize.
• Enhancing the effectiveness and range of activities of Cry
genes by domain engineering to produce chimeric proteins
• Looking beyond the large family of Bt genes to find other
insecticidal genes (vegetative insecticidal protein, Vip) that
could be used in place of Bt.
• Following integrated pest management (predators, adjacent
plant species, crop rotation, chemical sprays) practice: rotating
Bt crop with non Bt crop, avoiding growing different Bt crops
within the migration distance of pests common to both.
• Applying high dose / refuge approach to inhibiting the build
up of insect resistance to Bt

Breeding for abiotic resistance
• Phenotypic performance of a population is determined by
genotype, environment and G x E interaction.
• In an optimal environment, there is no interference by any
environmental factors (stress free environment).
• Any factor of the environment interferes with the complete
expression of genotypic potential, it is called stress.
• The abiotic stress are: drought, heat, cold and mineral (salinity,
acidity, mineral deficiency, oxidation and mineral toxicity)
• Yield loss can be minimised by crop management and development
of resistant/tolerant varieties. Stress during reproductive phase
leads greater yield losses that that of during earlier growth phase.
Suitable soil amendments should be used to improve the soil status
of the field.
• Different varieties of a crop also show large differences in their
ability to withstand a given stress.
• Different growth stages of crop may show large differences in their
tolerance to concerned stress (seedling...........heading).

Underlying principle
Yield =T ×WUE ×HI
where T =total seasonal crop transpiration,
WUE =crop water use efficiency, and
HI =crop harvest index.
This relationship clearly indicates that the focus
in breeding for drought resistance should be
on water use (efficient water use), rather
than water saving.

Common stresses
• Drought
• Heat
• Cold
• Salinity
• Mineral toxicity
• Mineral deficiency
• Oxidation
• Water logging

Criteria for the development and use of screening
test
• Genetic variation in the germplasm pool
• Trait with high heritability than yield per
se
• Trait should be correlated with a yield
based stress resistance index
• Trait should enhance the yield
• Screening test should be easy, rapid and
economical to apply

Drought resistance
• Drought means the inadequacy of water
availability.
• Moisture stress is the inability of plants to
meet the evapotranspirational demand.
• Drought resistance is the mechanism causing
minimum loss of yield in a drought
environment relative the maximum yield in a
optimal environment of the crop.

Which genotype is the most drought tolerant and which one is
the most sensitive?
Geno
type
Yield W/o
Drought
Q/ha
Yield in
drought
Q/ha
Loss
Q/ha
A 45 30 15
B 50 45 05
C 60 50 10
D 70 30 40
E 30 20 10

Selection could be based on
• Selection for survival
• Selection for yield
• Selection for traits contributing to stress resistance

Mechanisms of drought resistance
(i) drought escape: development of earlier maturing variety, crop
management
(ii) dehydration avoidance: It is the ability of a plant to retain a
relatively higher level of hydration under soil or atmospheric stress
conditions. It is achieved by
• Reduced transpiration: water saver plants
– Stomatal sensitivity (stomata closing)
– Osmoregulation (maintain turgor pressure)
– Cuticular wax
– Abscisic acid
– Leaf characteristics (pubescence, leaf angle and leaf movement, leaf
rolling)
• Increased water uptake: water spender plants
Root characteristics
– Deep root system
– Root length density
– Root hydraulic resistance

(iii) dehydration tolerance
• Maintenance of member integrity
• Plant growth
– Seed germination
– Seedling survival
– Seedling growth
– Presence of awns
– Stem reserves
– Proline accumulation

(iv) Recovery:
Because drought varies in
duration, some species are able
to rebound (recover) after a brief
drought episode. Traits that
enhance recovery from drought
include vegetative vigor, tillering,
and long growth duration.

Sources of drought resistance
• Cultivated species
• landraces
• wild relatives and wild forms
• transgenes

Attributes of Selection criteria
• Easy to estimate/score
• High heritability
• Large genetic variability for the trait
• Association of trait with drought resistance
• Positive association with yield under stress

Selection criteria: Dehydration Avoidance
• Leaf rolling
• Leaf firing
• Canopy temperature
• Leaf attributes (pubescence, heavy
glaucous, erect)
• RWC
• Root characteristics

Selection criteria: Dehydration Tolerance
• Seed germination
• Seedling growth under PEG stress
• Growth under stress
• Plant phenology (delayed or accelerated
heading/flowering, synchronous flowering,
shorter pollination time interval)
• Grain filling by translocated stem reserve
• Cellular membrane stability under stress
• Water use efficiency
• Canopy temperature
• Presence of awns

Drought Traits in general
• Cuticular wax Leaf pubescence
• Leaf rolling Leaf firing Erect leaf
• Leaf colour(1/3rd yellow in wheat and barley)
• Root length and density, production of lateral roots
• Presence of awns Production of abscisic acid
• Low canopy temperature High CT depression
• Chlorophyll content Stomata closing
• STI and SSI RWC
• Shorter plant height (stem reservation utilization): shoot
senescence, export of stored carbohydrates into grains.
• Flag leaf duration and senescence (Stay green colour)
• Grain filling rate & duration Short growth duration (EF)
• Short anthesis to pollination time interval, Small LAI

• CTD = (Ambient T – Canopy T)
• ST = (Yp – Ys)
• MP = (Yp + Ys)/2
• GMP = (Yp * Ys)0.5
• RWC = (Fw - Dw) / (Tw - Dw)
• STI = (Yp * Ys) / (Yp)2, higher the STI
value higher the resistance
• SSI = (1 – Ys / Yp) / D; D = (1 – Xs / Xp)
where D is stress intensity.
SSI (≤0.5: Highly tolerant, ˃0.5 – ≤1.0:
Moderately Tol., ˃ 1.0: susceptible)

Drought hardening
• It refers to improved resistance of a genotype to drought
as a consequence of a seed/seedling treatment. The
various hardening treatments are classified into two
groups (i) pre-sowing and (ii) post sowing treatments.
• Pre-sowing treatments: These treatments are applied to
seeds before they are planted in the field. A sample
seeds treatment consists of soaking the seeds for 24
hours in water, and sun drying them; these seeds are
then sown in the field.
• Post sowing treatments: These treatments are applied to
young seedlings. A mild moisture stress applied to young
seedlings is reported to improve their drought resistance
during later stages of growth.

Approaches for breeding drought
resistance
1. indirect breeding and 2. direct breeding
Indirect breeding
• In this strategy, the breeder exposes the genotypes
to an environmental stress, even though they are
not being directly evaluated for environmental
stresses.
• Indirect selection pressure is applied to these
genotypes by conducting performance trials at
locations where stress conditions exist. This
approach is not advisable if the cultivars to be
released are not intended for cultivation in the
location where the evaluation was conducted.

2. Direct breeding
Direct selection for drought is best
conducted under conditions where the
stress factor occurs uniformly and
predictably.

Direct selection Approaches
• Field selection
Water requirement is variable from year to year, and may be
sufficiently severe in one year to cause a loss of breeding
materials. Further, drought in different seasons can occur at
different growth stages. Without special management for stress,
inconsistencies in the field may result in inconsistent selection
pressure from one cycle to the next. The ideal field selection site
would be the desert, where irrigation may be used to dispense
water at desired rates.
• Selection based on yield per se
The concept of genotype × environment (G×E) is used to
evaluate genotypes at the end of a breeding program. The
desired genotype is one with minimal G×E inter-action, and
stable yield in its target environment and across other
environments. Using MAB, QTLs are selected.

• Selection based on developmental traits: root
size and development, and stem reserve
utilization (spraying plants with oxidizing
chemicals eg, potassium iodide)
• Selection based on assessment of plant water
status and plant function: leaf rolling, leaf
desiccation, leaf tip burning, canopy
temperature, cell membrane stability and
chlorophyll fluorescence
• Selection under managed stress environments:
With the help of Rainout shelter

Breeding Methods
• In breeding for drought resistance, breeders may select for
early maturity for use in avoiding the stress. Also, genotypes
with proven drought resistance may be used in hybridization
programs to transfer the resistance genes into superior
cultivars. The selection methods discussed and the various
breeding methods previously discussed are used in the
selection process.

Breeding Methods
• Selection
• Introduction
• Germplasm Collection
• Hybridization followed by Back crossing
• Mutation
• Somaclonal Selection
• Genetic Engineering

Steps
• Perform multi location trials under stress condition to identify
stable and drought resistant lines to be used as parents for
hybridization
• Hybridize selected drought resistant line with mostly adapted
cultivar
• Grow F1, F2 and F3 under non stress conditions and F3
individual plant progenies are evaluated for yield attributes and
selection is done
• Evaluate F4 progenies under stress and non stress conditions.
Identify resistant progenies and grow in F5.
• Select best lines are selected and perform multi location trials
• Release best line(s) for commercial cultivation

Estimate STI and SSI
SN
Genotypes
Non-stressed condition
Grain yield (kg/plot)
Stressed condition
Grain yield
(kg/plot)
1
Pasang Lhamu 25 20
2
Godawari 25 15
3
WK1701 32 25
4
WK1544 15 8
5
WK1204 30 25
6
WK1720 29 19
7
WK1777 28 18
8
3EBWYT 513 40 35
9
3EBWYT 529 35 30
10
2EBWYT 516 17 13

Estimate RWC
S N Genotypes Turgid
Weight (g)
Fresh weight
(g)
Dry weight
(g)
1
WK1701 30 20
15
2
WK1544 25 20
15
3
WK1204 30 25
20
4
WK1720 20 15
14
5
WK1777 15 12
10

Breeding for Heat stress
• T is basic to life processes, which increase
with T within a limited range.
• Effect is expressed as Q10, which is the ratio
of the rate at one T to that at a T 10 0C lower.
• Normal growth and development of each
genotype is in optimal range of T.
• When T moves beyond optimal range, it
generates T stress.
• T stress may be grouped as heat, chilling and
freezing stresses

Heat stress
• The adverse effects on plants of
temperature higher than the
optimal is considered as heat stress.
• Heat would affect cell and tissue
survival, growth and development
and physiological processes of the
plants.

Cell and tissue survival
• Organs due to lack of transpirational
cooling (twigs, fruits, trunks)
• Surface T reaches 48-50 0C
• Seedlings are more prone to such
injuries
• Reproductive processes are especially
sensitive to heat

Growth and Development
• Phenological events are accelerated by the
cumulative effect of T, which is referred as heat
units or heat sums.
• Effects of heat depends both on T and the duration
of exposure at that T
• Acceleration of plant development by heat reduces
yield, organ size, grain filling duration, grain size
and also premature senescence.
• The different stages of growth and development
differ in their sensitivity to heat stress (Wheat:
spike initiation to anthesis)

• The product of days and temperature is
known as temperature sum or thermal unit
(day degrees, d OC)
• Maize crop grown at a constant temperature
of 25 OC and has a threshold temperature 10
OC will start flowering after 50 days. The
temperature sum required for this crop is 750
d OC. Days to anthesis is calculated by
temperature sum/(field temperature-
threshold temperature).
• If grown at a constant 35 OC, starts flowering
after [750 dOC/(35 – 10 OC)] days. It means it
starts flowering after 30 days.

Physiological Effects
1. Respiration (R) : R = A - P
• Two types: MR and GR
• Maintenance respiration (Rm) : energy
required to maintain a biological entity and
support its functioning and
• Growth respiration (Rg) : energy required for
biochemical conversion of glucose into
structural plant materials, end products.
• Increase in MR leads decrease in growth that
ultimately results in decrease in yield.

• (Rm) = 0.03Wleaf + 0.015 Wstem + 0.015
Wroot + 0.01 Wstorage
• Values of maintenance coefficient,
reference temperature for C3 and C4 crops
are 20-25 and 25-30 OC respectively.
• Temperature correction coefficient (TC) =
Q10
(T-Tref)/10
• Where Q10 commonly equals 2, means the
rate of process considered doubles at a
10O increases.

Factors affecting respiration
i) Temperature
ii) Oxygen
iii) CO2
iv) Inorganic salts
v) Water
vi) Light
vii) Injury

• Conversion costs (g glucose/g dry matter)
• Fats: 3.189, carbohydrates: 1.275,
proteins: 1.92, organic acids: 0.954,
minerals: 0.12 and lignin: 2.231
• Conversion factors, CF (g dry matter /g
glucose)
– Non-legumes: leaf=0.68, stem= 0.66 and root=
0.68
– Legumes: leaf=0.59, stem= 0.62 and root= 0.64
– Storage organs: bean= 0.57, maize= 0.67, potato=
0.78, wheat= 0.70,
• soybean= 0.46 and stem wood= 0.63

• Maintenance coefficient (MC) at 20 oC
(kg glucose/kg dm/day) and CVF (kg
production/kg glucose) for different
crops
• Crop group MC CF
• Root/tubers 0.01 0.75
• Cereals 0.015 0.7
• Protein rich seed crops 0.025 0.65
• Oil rich seed crops 0.03 0.5

Physiological Effects …………….
2. Photosynthesis/Assimilation
• Photo system II: photolysis of water and
reduction of CO2.
• Enzymes destabilized of chloroplasts

Factors governing photosynthesis
i) Light intensity
ii) CO2 concentration
iii) temperature
iv) leaf age
v) water status of leaf
vi) nitrogen status of leaf
vii)CH2O status of leaf
viii) pests/diseases

Physiological Effects ………….
3. Photosynthetate translocation: reduce
grain growth
4. Protein denaturation
5. Membrane composition and stability :
lipids becomes increasingly liquid.
6. Heat shock proteins : beneficial, heat
tolerance

Heat resistance
Heat stress resistance may be
defined as the ability of some
genotypes to perform better than
others when they are subjected to
the same level of heat stress.

Mechanisms of Heat resistance
1. Heat avoidance: The ability of a genotype to
dissipate the radiation energy and, there by,
to avoid a rise in plant T to a stress level.
• Primary mechanism: Transpiration.
• Leaf surface attributes: pubescence,
glaucousness, bark are the components of
heat avoidance.

2. Heat tolerance
Ability of some genotypes to
perform/withstand better than others
when their internal Ts are comparable and
in the realm of heat stress is called heat
tolerance.

Components of Heat tolerance
• Membrane stability: lipid fluidity and
electrolyte leakage
• Thermosensitivity of Photosystem II
• Photosynthetate translocation
• Stem reserve mobilization
• Osmoregulation (proline, glycine betaine
protects several enzymes from heat
inactivation in vitro)

Selection criteria for Heat resistance
• Growth under heat stress
• Yield under heat stress
• Flower, fruit, seed formation, grain filling and
pollen fertility
• Seed germination under heat stress
• Recovery after heat stress
• Sensitivity of photosynthetic process and
chloroplast
• Membrane stability following heat shock
• Membrane thermostability

Heat Injury (%) =
[1-{ (T1/T2)/(C1/C2)}]
x 100

Selection Of Traits for Heat Resistance
• Cuticular wax Leaf pubescence
• Seed germination Seedling survival
• Erect leaf Presence of awns
• Production of heat shock proteins
• Low canopy temperature High CT depression
• RWC Chlorophyll content
• STI and SSI Stomata closing
• Shorter plant height (stem reservation)
• Flag leaf duration and senescence
• Grain filling duration and rate
• Anthesis to Pollination time interval
• Earlier anthesis: high development rate

Selection Of Traits for Heat Resistance
Contd…………..
• Membrane stability Recovery after stress
• Pollen viability/fertility Pod/fruit/seed set
• Thick bark Stem reserve mobilization
• Photosynthate translocation: callose formation
in phloem and inhibit translocation by heat
• Osmoregulation: proline, glycine-betaine have
protective role. Protect several enzymes from
heat inactivation.

Breeding Methods
• Selection
• Introduction
• Hybridization followed by back crossing
• Mutation
• Somaclonal Variation
• Genetic Engineering
• Germplasm Collection

Some Formulas
• TAR = T / Ag (Kg H2O transpired/Kg CO2 fixed)
• WUE = CVF x (30/44 x Ag – W x MC)
• WUE = (ʌW/ʌt) / T
• WUE = {HI x CVF x (30/44 x Ag – W x MC)}/
T + (E + D + R)
• WUE = W(dry matter) /T(crop water use)
• TC = Kg H2O transpired/Kg DM produced)
• Yield = T x WUE x HI

• 1 mole CH2O = 470 KJ
• 1 mole light quanta = 210 KJ
• 1 mole CO2 = 44 g
• LUE in the absence of photorespiration
= 44 g CO2 / 8 x 210 KJ
• 8 light quanta + H2O + CO2 = CH2O + O2
• 1 Kg H2O /m2= a water layer of 10-3 or
1 mm.
• 1 mm = 10,000 l /ha.

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