MUlTIPLE DISEASE RESISTANCE IN PLANTS
K . Kuralarasi ,
M.SC (Ag) – II nd year,
Dept of Plant pathology
Chairman :
Dr. t. Sivakumar,
Associate Professor,
DEpt of plant pathology.
Co- chairman:
Dr. P.BALABASKAR,
Associate Professor
DEpt of plant pathology.
Dr . K. R.SARAVANAN,
Assistant Professor,
DEpt of Genetics and plant breeding
INTRODUCTION
Plant Disease : Any abnormal condition that alters
the appearance or function of a plant
• PDR - Protection of plants form pathogens by
 Pre formed structures, chemicals, toxins and
secondary metabolites
 Response of immune system thus by reducing
the virulence of pathogen (growth, reproduction
and Sporulation)
PLANT DISEASE RESISTANCE
GENE FOR GENE HYPOTHESIS
Proposed by H.H. Flor
in 1946
First identified in
Flax rust incited by
Melampsora lini
 Plant host resistance
 Coined the term Vertifolia effect
 Founder of horizontal and vertical
resistance
 “Plant disease epidemics and control”
- 1963
 “Father of Epidemiology”
CONTRIBUTIONS OF J.E.VANDER PLANK
TYPES OF RESISTANCE
Non host
resistance
True
resistance
Apparent
resistance
Plant defense
mechanism
Vertical Resistance Horizontal
resistance
Disease
escape
Disease
Tolerance
Pre infectional defense
mechanism
Post infectional
defense mechanism
Morphological and
structural defense
mechanism
Bio chemical
defense
mechanism
Morphological and
structural defense
mechanism
Bio chemical
defense mechanism
STRUCTURAL DEFENSE MECHANISM
 The surface of the plant or host is first line of defense
against the pathogen.
 The pathogen must adhere to the surface and penetrate ,
if it is to cause infection
 Structural defense mechanism are mainly two type :
a. Pre existing structural defense mechanism
b. Post inflectional or induced structural defense
mechanism
PRE EXISTING STRUCTURAL DEFENSE
INDUCEDSTRUCTURAL DEFENSE
 Wax
 Thick cuticle
 Thickness and toughness of the outer wall of epidermal
cells
 Stomata
 Sclerenchyma cells
 Lenticel
 Cellular defense structure :
Hyphal sheathing
 Histological defense structure :
a) Formation of corky layer
b) Formation of Abscission layer
c) Formation of tyloses
d) Deposition of gums
PRE EXISTING STRUCTURAL DEFENSE
It includes :
• Amount and quality of wax and cuticle
• shapes , size and locations of natural openings
• Presence of thick walled cells in the tissues of the plant that hinder
the advance of pathogen
WAX
• It is the mixture of long
chain of apolar lipid
• It forming a protective
coating on plant leaves and
fruit
• Synthesized by epidermis
• Extremely hydrophobic
• Eg.Presence of wax on
Amaranthus leaf surface
prevent white blister caused
by Albugo candida (Mario
serrano 2014)
CUTICLE & EPIDERMAL CELL
 Ex: Disease resistance in Barberry species infected with Puccinia graminis tritici has
been attributed to the tough outer epidermal cells with a thick cuticle .
 In linseed , Cuticle acts as a barrier against Melampsora lini
SCLERENCHYMA CELLS
It composed of thickened
walls of lignin.
Sclerenchyma cells is
present in stem and leaf
veins
Brittle cells help in
mechanical support of the
plant
Effectively block the spread
of some fungal and bacterial
pathogens that cause
angular leaf spot.
Ex: Beet varieties – Cercospora beticola
(Sanjeet kumar 2013)
STRUCTURE OF NATURALOPENINGS
 Most of pathogen enter plants
through natural opening.
 Some pathogen like stem rust of
wheat (Puccinia graminis
f.sp.tritici) can enters its host
only when the stomata are open
 Structure of stomata provides
resistance to penetration by
certain plant pathogenic bacteria
A. Stomata:
LENTICELS
 Lenticels are opening on
fruit, stem and tubers that
are filled with loosely
connected cells that allow the
passage of air
 Shape and internal structure
of lenticels can increase or
decrease the incidence of
diseases.
 Ex. Small and suberized
lenticels will offer resistance
to potato scab pathogen ,
Streptomyces scabies.
(Sanjeet kumar 2013)
POST INFECTIONAL / INDUCED STRUCTURALDEFENSE
MECHANISM
Most pathogen manage to penetrate their hosts through
wounds and natural opening and to produce various
degree of infection.
Pathogen penetration through the host surface induced
the structural defense mechanism in the host cells
These may be regarded as :
 Histological defense barriers (Cork layer, Abscission
layers and Tyloses formation)
 Cellular defense structures (Hyphal sheathing )
HISTOLOGICAL DEFENSE MECHANISM
 Infection by Fungi , bacteria , some
viruses and nematodes induce plants to
form several layers of cork cells beyond
the point of infection
 These cork cells inhibits the further
invasion by the pathogen beyond the
initial lesion and also blocks the spread
of toxin substance secreted by the
pathogen
 It also stop the flow of nutrients and
water from the healthy to the infected
area and deprive the pathogen of
nourishment
CorkY layer
Ex: potato tubers infected by Rhizoctonia
(Sanjeet kumar 2013)
ABSCISSIONLAYERS
 An abscission layer consists of a gap formed between infected and healthy cells of leaf
surrounding the locus of infection
 Due to the disintegration of middle lamella of Parenchymatous tissue.
 Gradually , infected area shrivels , dies and sloughs off , carrying with it the pathogen
 Abscission layers are formed on young active leaves infected by Fungi, bacteria or viruses.
Ex: Xanthomonas pruni on peach leaves. (Young et al. 2002)
TYLOSES
 Tyloses are the overgrowths of the Protoplast of adjacent living
parenchymatous cells, which protrude into xylem vessels through pits.
 Tyloses have cellulosic walls
 It formed quickly ahead of the pathogen and may clog the xylem vessels
completely blocking the further advance of the pathogen in resistant varieties
Ex: Tyloses form in vessels of most plants under invasion by most of the vascular
wilt pathogens (Sauban Musa Jibril et al. 2016)
GUM DEPOSITION
 Various types of gums are produced by many plants around lesions after
infection by pathogen or injury
 Gums secretion is most common in stone fruit trees
 Generally these gums are exudated by plant under stressed condition
 Gummosis is the process in which gum produced by the plants and trees
(Sauban Musa Jibril et al. 2016)
CELLULAR DEFENSE STRUCTURE
Eg :Hyphal sheathing is observed in flax infected with
Fusarium oxysporum f. sp lini (Raheleh et al. 2016)
Hyphal sheathing
BIOCHEMICAL DEFENSE MECHANISM
Pre existing chemical defense :
1. Inhibitors :
Released by plant in it’s environment
Ex. Chick pea - Malic acid – Ascochyta rabiei
Citrus - Cutin acid – Gleosporium limetticola
2. Present in plant cells before infection
1. Phenolics :
Tannins – Botrytis sp.
2. Phytoanticipin - Tomatin in tomato , Avinasin in oats
3. Hydrolytic enzymes – Glucanase , Chytinase
4. Lectins
Induced chemical defence :
 Hypersensitivity response (HR)
 Production of Antimicrobial substrates
i. Phytoalexins
ii. PR proteins (Agrios 2005)
PLANT IMMUNE SYSTEM
Non Specific Specific
• Based on recognition of PAMP
• Its also known as PAMP triggered
immunity (PTI)
• Based on recognition of Pathogen
effectors
• Its also known as effector triggered
immunity (ETI)
(Dangal and Jones 2001)
MULTIPLE DISEASE RESISTANCE (MDR)
Multiple diseasesusceptibility (MDS)
The resistant plants are susceptible to two more diseases / plant
susceptibility to two or more diseases to which the plant species
normally resistant
( Tyr Wiesner-Hanks and Rebecca Nelson 2016)
Host plant resistance to two or more plant diseases
2 types, viz.,
 Qualitative
 Quantitative
MULTIPLE DISEASE RESISTANCE AT THE WHOLE-GENOME
SCALE
MDR is of clear evolutionary importance and agricultural interest
for example, potato is attacked by least 12 major diseases and pests in
Europe
( Jellis 1992)
Wheat plants are often infected by multiple pathogens at a given time
(Gurung et al. 2012)
Resistance to multiple diseases is therefore of great importance to plant
pathologists and breeders for controlling diseases and losses
Resistance to multiple diseases was documented in cowpea in 1902
(Webber and Orton 1902)
Journal of Plant Registrations (JPR) having 70 germplasms with
resistance to multiple diseases and 30 germplasm with resistance to
single disease ( Tyr Wiesner-Hanks and Rebecca Nelson 2016)
MULTIPLE DISEASE
RESISTANCE
• MDR at whole genome level
• MDR at loci level
• MDR at gene level insights
MDR AT WHOLE GENOME SCALE
 Germplasm screening
 Multi environment trials
 Screening of wild relatives
 Structured populations
GERMPLASM SCREENING
Crop improvement programs routinely involving in
germplasm screening collections for resistance to multiple
disease
MDR varies highly from study to study often even across
in the studies of same host – pathogens systems.
Ex:
Spring wheat landraces are screened for five leaf spot
diseases, resistance were correlated for 11 of the 15 pairs of
pathogens tested, but less than 1% of accessions shows
resistant to three or more diseases.
(Gurung et al. 2014)
MULTI ENVIRONMENT TRIALS
 Most of the screening studies are take place under controlled
conditions at a single location.
 Multi environment field trails are done to assess the stability
of resistance against multiple pathogen species and genera.
Ex:
In Fava bean, 43 accessions were screened to two diseases
of these 11 accessions were shows stable resistance to both
diseases were identified and these are confirmed under
controlled conditions.
(Fernandez et al. 2011)
SCREENING OF WILD RELATIVES
Wild or cultivated crop species may be the source for
multiple disease resistance
Screening of wild crop relatives can capture high effective
form of multiple disease resistance.
Ex:
• An identified interspecific hybrid potato clone shows
resistance to 5 diverse diseases .
• Wild progenitor of Barley accessions were resistance to 6
fungal pathogens
(Fetch et al. 2003)
STRUCTURED POPULATIONS
 Population structure refers to the patterns of genetic
relatedness among the population of same species
Ex:
Population structure largely explained resistance in
correlation of two maize diversity panels were the
tropical lines shows more resistant then temperate lines .
(Poland 2010)
MULTIPLE DISEASE RESISTANCE AT THE LOCUS LEVEL
QUANTITATIVE TRAIT LOCI
 Term coined by Gelderman (1975)
 Quantitative trait locus is a locus that correlates with
variation of a quantitative trait in the phenotype of a
population of organisms.
 Process of constructing linkage maps and conducting
QTL analysis is known as QTL Mapping
Examples of MAS applications in rice (adapted from Collard et
al. 2008) J. Plant Breed. Genet. 01 (02) 2013. 90-109
98
trait Gene(s)/
QTL(s)
Type/name of
marker(s) used
Reference Remarks
1
Bacterial blight
(BB) resistance
Xa21 STS (pTA248) Ronald et al. 1992 MAS applied for
MABB
Bacterial blight
(BB) resistance
Xa4, xa5 &
Xa10
Gene linked
RFLP and RAPD
markers
Yoshimura et al. 1995 MAS applied for
gene pyramiding
Bacterial blight
(BB) resistance
Xa4, xa5,
xa13 &
Xa21
STS for Xa4
CAPS for xa5
(RG556+DraI)
CAPS for xa13
(RG136+HinfI)
STS for Xa21
(pTA248)
Huang et al. 1997 MAS applied for
gene pyramiding
Bacterial blight
(BB) resistance
xa13 &
Xa21
CAPS for
xa13
(RG136+Hi
nfI)
STS for
Xa21
(pTA248)
Pandey et al.2013 Improved the two
traditional BB-susceptible
Basmati varieties (Taraori
Basmati and Basmati
386)
Bacterial blight
(BB) resistance +
Blast resistance
Xa21& Pi54 STS for
Xa21
(pTA248)
SSR for
Pi54
(RM206)
Hari et al. 2013 Marker-assisted
introgression of bacterial
blight and blast
resistance into IR 58025B,
an elite maintainer line of
rice
Bacterial blight
(BB) resistance
Xa4, xa5,
xa13 &
Xa21
STS for Xa4
CAPS for
xa5
(RG556+Dr
aI)
CAPS for
xa13
(RG136+Hi
Dokku et al. 2013 Three resistance genes
i.e. xa5, xa13 and Xa21
were transferred from
IRBB 60 through MABC to
supplement the Xa4 gene
present in Tapaswini, an
elite cultivar having a
wide coverage
GENE-LEVEL INSIGHTS
 Recognition of Conserved Signals
 Hormone Signaling
 Sugar Signalling and Partitioning
 Cell Death and the Hypersensitive Response
 Oxidative and Chemical Stress
 Antimicrobial Peptides
RECOGNITION OF CONSERVED SIGNALS
 Disruption of recognition pathways can lead to the loss of
multiple resistance and successful pathogens have evolved
to rapidly suppress the basal resistance provided by PAMP
triggered immunity .
 Ex: Arabidopsis RPM1 gene shows resistance to strains of
Pseudomonas carrying either of two Avr genes
(Grant et al. 1995 )
 Once threats having recognized , plants shared signaling
pathways to initiate defense response .
 Salicylate , Jasmonate , Ethylene , Abscisic acid and cross
talk between these pathways are the response to biotic and
abiotic stress.
Ex:
In Rice GH3-2 locus mediate resistance to Xanthomonas
oryzae & Magnaporthae grisea was found to encode a
synthetase that produce the main form of Auxin in rice
(Fu et al. 2011)
HORMONE SIGNALING
SUGAR SIGNALLING AND PARTITIONING
Changing concentrations or ratios of sugars in plant tissues
can induce plant defense genes , influence plant hormone
pathways and induce resistance to various disease.
Ex : The resistance allele of wheat Lr 67 gene shows
resistance to leaf rust , Stripe rust , stem rust & powdery
mildew encodes Hexose transporter that inhibits Hexose
uptake from the Apoplast by the host cells .
(Moore et al. 2015 )
CELL DEATH ANDTHE HYPERSENSITIVE RESPONSE
 Plant cell death is an important defense mechanism against
biotrophic pathogens but it act as a gateway to infection
for necrotrophic pathogens.
 Ex : The most famous example of this the recessive mlo
gene in barely, which provides resistance to several
biotrophic pathogens.
(Hollricher et al. 2000)
OXIDATIVE ANDCHEMICALSTRESS
 Plants begin to form a wide array to Reactive oxygen
species(ROS) in a process known as Oxidative burst .
 These ROS strengthen plant cell walls, serve as a signal to
induce the disease defense response and potentially create
a hostile environment for invading pathogens.
 Necrotrophic pathogens, in turn , can elicit host production
of ROS and secrete toxic compounds to kill host tissue.
 Mitigating the chemical and oxidative stress is critical for
maintaining plant health.
(Torres et al. 2006)
ANTIMICROBIAL PEPTIDES
 Plants, animals, bacteria and fungi produce peptides with
broad antimicrobial activity.
 Antimicrobial peptides vary greatly in structure , targets
and efficacy.
 Small, cysteine-rich antimicrobial peptides that have long
recognized as an ancient, basal component of plant
defence against diseases.
 Ex. Pea Pi39 defensing conferring resistance to Fusarium
solani f.sp. pisi and Ascochyta blight.
(Coyne et al. 2015)
CASE STUDY
Multiple disease resistance in plants
Multiple disease resistance in plants
Multiple disease resistance in plants
Multiple disease resistance in plants
Multiple disease resistance in plants
Multiple disease resistance in plants
Multiple disease resistance in plants
Multiple disease resistance in plants

Multiple disease resistance in plants

  • 2.
    MUlTIPLE DISEASE RESISTANCEIN PLANTS K . Kuralarasi , M.SC (Ag) – II nd year, Dept of Plant pathology Chairman : Dr. t. Sivakumar, Associate Professor, DEpt of plant pathology. Co- chairman: Dr. P.BALABASKAR, Associate Professor DEpt of plant pathology. Dr . K. R.SARAVANAN, Assistant Professor, DEpt of Genetics and plant breeding
  • 3.
    INTRODUCTION Plant Disease :Any abnormal condition that alters the appearance or function of a plant
  • 5.
    • PDR -Protection of plants form pathogens by  Pre formed structures, chemicals, toxins and secondary metabolites  Response of immune system thus by reducing the virulence of pathogen (growth, reproduction and Sporulation) PLANT DISEASE RESISTANCE
  • 6.
    GENE FOR GENEHYPOTHESIS Proposed by H.H. Flor in 1946 First identified in Flax rust incited by Melampsora lini
  • 7.
     Plant hostresistance  Coined the term Vertifolia effect  Founder of horizontal and vertical resistance  “Plant disease epidemics and control” - 1963  “Father of Epidemiology” CONTRIBUTIONS OF J.E.VANDER PLANK
  • 8.
    TYPES OF RESISTANCE Nonhost resistance True resistance Apparent resistance Plant defense mechanism Vertical Resistance Horizontal resistance Disease escape Disease Tolerance Pre infectional defense mechanism Post infectional defense mechanism Morphological and structural defense mechanism Bio chemical defense mechanism Morphological and structural defense mechanism Bio chemical defense mechanism
  • 9.
    STRUCTURAL DEFENSE MECHANISM The surface of the plant or host is first line of defense against the pathogen.  The pathogen must adhere to the surface and penetrate , if it is to cause infection  Structural defense mechanism are mainly two type : a. Pre existing structural defense mechanism b. Post inflectional or induced structural defense mechanism
  • 10.
    PRE EXISTING STRUCTURALDEFENSE INDUCEDSTRUCTURAL DEFENSE  Wax  Thick cuticle  Thickness and toughness of the outer wall of epidermal cells  Stomata  Sclerenchyma cells  Lenticel  Cellular defense structure : Hyphal sheathing  Histological defense structure : a) Formation of corky layer b) Formation of Abscission layer c) Formation of tyloses d) Deposition of gums
  • 11.
    PRE EXISTING STRUCTURALDEFENSE It includes : • Amount and quality of wax and cuticle • shapes , size and locations of natural openings • Presence of thick walled cells in the tissues of the plant that hinder the advance of pathogen WAX • It is the mixture of long chain of apolar lipid • It forming a protective coating on plant leaves and fruit • Synthesized by epidermis • Extremely hydrophobic • Eg.Presence of wax on Amaranthus leaf surface prevent white blister caused by Albugo candida (Mario serrano 2014)
  • 12.
    CUTICLE & EPIDERMALCELL  Ex: Disease resistance in Barberry species infected with Puccinia graminis tritici has been attributed to the tough outer epidermal cells with a thick cuticle .  In linseed , Cuticle acts as a barrier against Melampsora lini
  • 13.
    SCLERENCHYMA CELLS It composedof thickened walls of lignin. Sclerenchyma cells is present in stem and leaf veins Brittle cells help in mechanical support of the plant Effectively block the spread of some fungal and bacterial pathogens that cause angular leaf spot.
  • 14.
    Ex: Beet varieties– Cercospora beticola (Sanjeet kumar 2013) STRUCTURE OF NATURALOPENINGS  Most of pathogen enter plants through natural opening.  Some pathogen like stem rust of wheat (Puccinia graminis f.sp.tritici) can enters its host only when the stomata are open  Structure of stomata provides resistance to penetration by certain plant pathogenic bacteria A. Stomata:
  • 15.
    LENTICELS  Lenticels areopening on fruit, stem and tubers that are filled with loosely connected cells that allow the passage of air  Shape and internal structure of lenticels can increase or decrease the incidence of diseases.  Ex. Small and suberized lenticels will offer resistance to potato scab pathogen , Streptomyces scabies. (Sanjeet kumar 2013)
  • 16.
    POST INFECTIONAL /INDUCED STRUCTURALDEFENSE MECHANISM Most pathogen manage to penetrate their hosts through wounds and natural opening and to produce various degree of infection. Pathogen penetration through the host surface induced the structural defense mechanism in the host cells These may be regarded as :  Histological defense barriers (Cork layer, Abscission layers and Tyloses formation)  Cellular defense structures (Hyphal sheathing )
  • 17.
    HISTOLOGICAL DEFENSE MECHANISM Infection by Fungi , bacteria , some viruses and nematodes induce plants to form several layers of cork cells beyond the point of infection  These cork cells inhibits the further invasion by the pathogen beyond the initial lesion and also blocks the spread of toxin substance secreted by the pathogen  It also stop the flow of nutrients and water from the healthy to the infected area and deprive the pathogen of nourishment CorkY layer Ex: potato tubers infected by Rhizoctonia (Sanjeet kumar 2013)
  • 18.
    ABSCISSIONLAYERS  An abscissionlayer consists of a gap formed between infected and healthy cells of leaf surrounding the locus of infection  Due to the disintegration of middle lamella of Parenchymatous tissue.  Gradually , infected area shrivels , dies and sloughs off , carrying with it the pathogen  Abscission layers are formed on young active leaves infected by Fungi, bacteria or viruses. Ex: Xanthomonas pruni on peach leaves. (Young et al. 2002)
  • 19.
    TYLOSES  Tyloses arethe overgrowths of the Protoplast of adjacent living parenchymatous cells, which protrude into xylem vessels through pits.  Tyloses have cellulosic walls  It formed quickly ahead of the pathogen and may clog the xylem vessels completely blocking the further advance of the pathogen in resistant varieties Ex: Tyloses form in vessels of most plants under invasion by most of the vascular wilt pathogens (Sauban Musa Jibril et al. 2016)
  • 20.
    GUM DEPOSITION  Varioustypes of gums are produced by many plants around lesions after infection by pathogen or injury  Gums secretion is most common in stone fruit trees  Generally these gums are exudated by plant under stressed condition  Gummosis is the process in which gum produced by the plants and trees (Sauban Musa Jibril et al. 2016)
  • 21.
    CELLULAR DEFENSE STRUCTURE Eg:Hyphal sheathing is observed in flax infected with Fusarium oxysporum f. sp lini (Raheleh et al. 2016) Hyphal sheathing
  • 22.
    BIOCHEMICAL DEFENSE MECHANISM Preexisting chemical defense : 1. Inhibitors : Released by plant in it’s environment Ex. Chick pea - Malic acid – Ascochyta rabiei Citrus - Cutin acid – Gleosporium limetticola 2. Present in plant cells before infection 1. Phenolics : Tannins – Botrytis sp. 2. Phytoanticipin - Tomatin in tomato , Avinasin in oats 3. Hydrolytic enzymes – Glucanase , Chytinase 4. Lectins Induced chemical defence :  Hypersensitivity response (HR)  Production of Antimicrobial substrates i. Phytoalexins ii. PR proteins (Agrios 2005)
  • 23.
    PLANT IMMUNE SYSTEM NonSpecific Specific • Based on recognition of PAMP • Its also known as PAMP triggered immunity (PTI) • Based on recognition of Pathogen effectors • Its also known as effector triggered immunity (ETI) (Dangal and Jones 2001)
  • 24.
    MULTIPLE DISEASE RESISTANCE(MDR) Multiple diseasesusceptibility (MDS) The resistant plants are susceptible to two more diseases / plant susceptibility to two or more diseases to which the plant species normally resistant ( Tyr Wiesner-Hanks and Rebecca Nelson 2016) Host plant resistance to two or more plant diseases 2 types, viz.,  Qualitative  Quantitative
  • 25.
    MULTIPLE DISEASE RESISTANCEAT THE WHOLE-GENOME SCALE MDR is of clear evolutionary importance and agricultural interest for example, potato is attacked by least 12 major diseases and pests in Europe ( Jellis 1992) Wheat plants are often infected by multiple pathogens at a given time (Gurung et al. 2012) Resistance to multiple diseases is therefore of great importance to plant pathologists and breeders for controlling diseases and losses Resistance to multiple diseases was documented in cowpea in 1902 (Webber and Orton 1902) Journal of Plant Registrations (JPR) having 70 germplasms with resistance to multiple diseases and 30 germplasm with resistance to single disease ( Tyr Wiesner-Hanks and Rebecca Nelson 2016)
  • 26.
    MULTIPLE DISEASE RESISTANCE • MDRat whole genome level • MDR at loci level • MDR at gene level insights
  • 27.
    MDR AT WHOLEGENOME SCALE  Germplasm screening  Multi environment trials  Screening of wild relatives  Structured populations
  • 28.
    GERMPLASM SCREENING Crop improvementprograms routinely involving in germplasm screening collections for resistance to multiple disease MDR varies highly from study to study often even across in the studies of same host – pathogens systems. Ex: Spring wheat landraces are screened for five leaf spot diseases, resistance were correlated for 11 of the 15 pairs of pathogens tested, but less than 1% of accessions shows resistant to three or more diseases. (Gurung et al. 2014)
  • 29.
    MULTI ENVIRONMENT TRIALS Most of the screening studies are take place under controlled conditions at a single location.  Multi environment field trails are done to assess the stability of resistance against multiple pathogen species and genera. Ex: In Fava bean, 43 accessions were screened to two diseases of these 11 accessions were shows stable resistance to both diseases were identified and these are confirmed under controlled conditions. (Fernandez et al. 2011)
  • 30.
    SCREENING OF WILDRELATIVES Wild or cultivated crop species may be the source for multiple disease resistance Screening of wild crop relatives can capture high effective form of multiple disease resistance. Ex: • An identified interspecific hybrid potato clone shows resistance to 5 diverse diseases . • Wild progenitor of Barley accessions were resistance to 6 fungal pathogens (Fetch et al. 2003)
  • 31.
    STRUCTURED POPULATIONS  Populationstructure refers to the patterns of genetic relatedness among the population of same species Ex: Population structure largely explained resistance in correlation of two maize diversity panels were the tropical lines shows more resistant then temperate lines . (Poland 2010)
  • 32.
    MULTIPLE DISEASE RESISTANCEAT THE LOCUS LEVEL QUANTITATIVE TRAIT LOCI  Term coined by Gelderman (1975)  Quantitative trait locus is a locus that correlates with variation of a quantitative trait in the phenotype of a population of organisms.  Process of constructing linkage maps and conducting QTL analysis is known as QTL Mapping
  • 33.
    Examples of MASapplications in rice (adapted from Collard et al. 2008) J. Plant Breed. Genet. 01 (02) 2013. 90-109 98 trait Gene(s)/ QTL(s) Type/name of marker(s) used Reference Remarks 1 Bacterial blight (BB) resistance Xa21 STS (pTA248) Ronald et al. 1992 MAS applied for MABB Bacterial blight (BB) resistance Xa4, xa5 & Xa10 Gene linked RFLP and RAPD markers Yoshimura et al. 1995 MAS applied for gene pyramiding Bacterial blight (BB) resistance Xa4, xa5, xa13 & Xa21 STS for Xa4 CAPS for xa5 (RG556+DraI) CAPS for xa13 (RG136+HinfI) STS for Xa21 (pTA248) Huang et al. 1997 MAS applied for gene pyramiding
  • 34.
    Bacterial blight (BB) resistance xa13& Xa21 CAPS for xa13 (RG136+Hi nfI) STS for Xa21 (pTA248) Pandey et al.2013 Improved the two traditional BB-susceptible Basmati varieties (Taraori Basmati and Basmati 386) Bacterial blight (BB) resistance + Blast resistance Xa21& Pi54 STS for Xa21 (pTA248) SSR for Pi54 (RM206) Hari et al. 2013 Marker-assisted introgression of bacterial blight and blast resistance into IR 58025B, an elite maintainer line of rice Bacterial blight (BB) resistance Xa4, xa5, xa13 & Xa21 STS for Xa4 CAPS for xa5 (RG556+Dr aI) CAPS for xa13 (RG136+Hi Dokku et al. 2013 Three resistance genes i.e. xa5, xa13 and Xa21 were transferred from IRBB 60 through MABC to supplement the Xa4 gene present in Tapaswini, an elite cultivar having a wide coverage
  • 36.
    GENE-LEVEL INSIGHTS  Recognitionof Conserved Signals  Hormone Signaling  Sugar Signalling and Partitioning  Cell Death and the Hypersensitive Response  Oxidative and Chemical Stress  Antimicrobial Peptides
  • 37.
    RECOGNITION OF CONSERVEDSIGNALS  Disruption of recognition pathways can lead to the loss of multiple resistance and successful pathogens have evolved to rapidly suppress the basal resistance provided by PAMP triggered immunity .  Ex: Arabidopsis RPM1 gene shows resistance to strains of Pseudomonas carrying either of two Avr genes (Grant et al. 1995 )
  • 38.
     Once threatshaving recognized , plants shared signaling pathways to initiate defense response .  Salicylate , Jasmonate , Ethylene , Abscisic acid and cross talk between these pathways are the response to biotic and abiotic stress. Ex: In Rice GH3-2 locus mediate resistance to Xanthomonas oryzae & Magnaporthae grisea was found to encode a synthetase that produce the main form of Auxin in rice (Fu et al. 2011) HORMONE SIGNALING
  • 39.
    SUGAR SIGNALLING ANDPARTITIONING Changing concentrations or ratios of sugars in plant tissues can induce plant defense genes , influence plant hormone pathways and induce resistance to various disease. Ex : The resistance allele of wheat Lr 67 gene shows resistance to leaf rust , Stripe rust , stem rust & powdery mildew encodes Hexose transporter that inhibits Hexose uptake from the Apoplast by the host cells . (Moore et al. 2015 )
  • 40.
    CELL DEATH ANDTHEHYPERSENSITIVE RESPONSE  Plant cell death is an important defense mechanism against biotrophic pathogens but it act as a gateway to infection for necrotrophic pathogens.  Ex : The most famous example of this the recessive mlo gene in barely, which provides resistance to several biotrophic pathogens. (Hollricher et al. 2000)
  • 41.
    OXIDATIVE ANDCHEMICALSTRESS  Plantsbegin to form a wide array to Reactive oxygen species(ROS) in a process known as Oxidative burst .  These ROS strengthen plant cell walls, serve as a signal to induce the disease defense response and potentially create a hostile environment for invading pathogens.  Necrotrophic pathogens, in turn , can elicit host production of ROS and secrete toxic compounds to kill host tissue.  Mitigating the chemical and oxidative stress is critical for maintaining plant health. (Torres et al. 2006)
  • 42.
    ANTIMICROBIAL PEPTIDES  Plants,animals, bacteria and fungi produce peptides with broad antimicrobial activity.  Antimicrobial peptides vary greatly in structure , targets and efficacy.  Small, cysteine-rich antimicrobial peptides that have long recognized as an ancient, basal component of plant defence against diseases.  Ex. Pea Pi39 defensing conferring resistance to Fusarium solani f.sp. pisi and Ascochyta blight. (Coyne et al. 2015)
  • 43.