Plant disease resistance occurs through both pre-formed structures and infection-induced immune responses. There are two tiers of the plant immune system - pattern-triggered immunity (PTI) triggered by pathogen-associated molecular patterns (PAMPs), and effector-triggered immunity (ETI) triggered by recognition of pathogen effectors through resistance (R) proteins. Quantitative resistance involving multiple genes provides more durable resistance than major gene resistance. Genetic engineering and breeding can enhance crop disease resistance through introduction of R genes or resistance mechanisms.

1. “DISEASE RESISTANCE IN PLANTS”
Divakaran P
M.sc.Biochemistry &
Molecular biology
Pondicherry university.

2.  Disease The continuous abnormal functioning of an organism;
a disruption in the health of the organism.
 Effectors Pathogen proteins and small molecules that alter host–cell
structure and function.
 Effector-triggered immunity Direct or indirect recognition of
pathogen effectors by plant resistance (R) proteins that leads to the
activation of plant defense responses.
 Evolutionary arms race Evolutionary struggle between competing sets
of coevolving genes that develop adaptations and counteradaptations
against each other.
Glossary

3.  PAMP-triggered immunity First active defense response of
plants, also referred to as activation of basal defenses, after
perception of PAMPs by plant PRRs.
 Pathogen A disease-producing organism or biotic agent.
 Pathogen-associated molecular patterns Highly conserved
molecules associated with groups of microbes that are
recognized by pattern recognition receptors (PRRs) on plant
surfaces to activate the innate immune system.
 Plant immunity The inherent or induced capacity of plants to
withstand or ward off biological attack by pathogens.

4. Introduction
 Plant disease resistance protects plants from pathogens in two ways:
by pre-formed structures and chemicals, and by infection-induced
responses of the immune system. Relative to a susceptible
plant, disease resistance is the reduction of pathogen growth on or in
the plant (and hence a reduction of disease).
 while the term disease tolerance describes plants that exhibit little
disease damage despite substantial pathogen levels.
 Disease outcome is determined by the three-way interaction of the
pathogen, the plant and the environmental conditions (an interaction
known as the disease triangle).

5. (1) the pathogenic microbe must be virulent on a particular species
and cultivar of plant.
(2) the plant host must be susceptible to a particular
strain/isolate/biotype of a pathogen.
(3) environmental conditions including temperature, humidity, and availability
of nutrients must be suitable for the interactions that lead to disease. If a
pathogen requires an insect vector for dissemination or inoculation then a
fourth dimension is added (a plant disease pyramid).
 The plant disease triangle shows the three components
necessary for disease to occur:

6. Plant disease resistance is a complicated arms race between the plant and
pathogens. Bacteria, viruses and fungi evolve in lock-step with plants, creating
new ways to overcome new disease resistance strategies. Resistance to disease
has a foundation in the gene-for-gene model, a model that hypothesizes that
plants and pathogens have a molecular relationship with each other that
mediates pathogenicity.

7.  How do Pathogens Find and Enter the Plant?
 For a microbe to cause disease, it needs to come into direct contact with its
host plant, and often with a specific host plant tissue.
 Microbes are passively distributed from plant to plant by wind, splashing rains,
or insect vectors.
 However, nonpathogenic microbes, once deposited, do not have the capacity
to find wounds or natural openings on the plant surface, or to penetrate
preformed surface barriers such as a waxy cuticle and thick cell walls.
 Pathogens, however, have evolved diverse mechanisms to find and enter
plants to establish the disease.
 Once they reach the host plant, a pathogenic microbe may land on the part of
the plant suitable for infection, called the infection court. In other cases,
pathogens need to expend energy to move or grow toward the infection
court

10. The plant immune system carries two interconnected tiers of receptors, one
most frequently sensing molecules outside the cell and the other most
frequently sensing molecules inside the cell. Both systems sense the intruder and
respond by activating antimicrobial defenses in the infected cell and
neighboring cells. In some cases, defense-activating signals spread to the rest of
the plant or even to neighboring plants. The two systems detect different types
of pathogen molecules and classes of plant receptor proteins.
Plant immune system
 The first tier is primarily governed by pattern recognition receptors that are
activated by recognition of evolutionarily conserved pathogen or microbial-
associated molecular paterns (PAMPs or MAMPs). Activation of PRRs leads to
intracellular signaling, transcriptional reprogramming, and biosynthesis of a
complex output response that limits colonization. The system is known as
PAMP-Triggered Immunity or as Pattern-Triggered Immunity (PTI).

11. The second tier, primarily governed by R gene products, is often termed
effector-triggered immunity (ETI).
 ETI is typically activated by the presence of specific pathogen "effectors"
and then triggers strong antimicrobial responses (see R gene section
below).
 In addition to PTI and ETI, plant defenses can be activated by the sensing
of damage-associated compounds (DAMP), such as portions of the plant
cell wall released during pathogenic infection.

12.  Pattern-triggered immunity
 PAMPs, conserved molecules that inhabit multiple pathogen genera,
are referred to as MAMPs by many researchers.
 The defenses induced by MAMP perception are sufficient to repel
most pathogens.
 Effector triggered immunity
 Effector Triggered Immunity (ETI) is activated by the presence of
pathogen effectors. The ETI response is reliant on R genes,
 and is activated by specific pathogen strains. Plant ETI often causes
an apoptotic hypersensitive response.

13.  R genes and R proteins
 Plants have evolved R genes (resistance genes) whose products mediate
resistance to specific virus, bacteria, oomycete, fungus, nematode or insect
strains.
 R gene products are proteins that allow recognition of specific pathogen
effectors, either through direct binding or by recognition of the effector's
alteration of a host protein.
 Most plant immune systems carry a repertoire of 100-600 different R gene
homologs.
 R gene products control a broad set of disease resistance responses whose
induction is often sufficient to stop further pathogen growth/spread.

14.  Genetic resistance has been the mainstay of disease control for many crop
species. The two broad categories of host resistance are major gene resistance
and quantitative resistance.
 As discussed earlier, major gene resistance is primarily involved in ETI
whereas quantitative resistance involves basal defenses triggered by PTI,
recognizing that there are considerable overlaps in the mechanisms triggered
by ETI and PTI.
 Under strong directional selection, as in the case of major gene resistance,
one or a few adapted pathogen strains will predominate the pathogen
population, leading to severe epidemics.
 Use of Disease Resistance Gene for Pathogen Control

17.  Plant disease resistance genes (R genes) encode proteins that detect pathogens.
 R genes have been used in resistance breeding programs for decades, with
varying degrees of success.
 Recent molecular research on R proteins and downstream signal transduction
networks has provided exciting insights, which will enhance the use of R genes for
disease control.
 Numerous signal transduction components in the defense network have been
defined, and several are being exploited as switches by which resistance can be
activated against diverse pathogens.
 R genes encode putative receptors that respond to the products of ‘Avr genes’
(Avr, avirulence) expressed by the pathogen during infection.

18.  In many cases, a single R gene can provide complete resistance to one or more
strains of particular pathogen, when transferred to a previously susceptible plant
of the same species.
 For this reason, R genes have been used in conventional resistance breeding
programs for decades .
 The strong phenotypes and natural variability at R loci have also been exploited
by molecular geneticists to clone the R genes and investigate their molecular
modes of action.
 R gene-mediated resistance has several attractive features for disease control.

19.  Special level resistance
 In a small number of cases, plant genes are effective against an entire
pathogen species, even though that species that is pathogenic on other
genotypes of that host species.
 Examples include barley MLO against powdery mildew ,wheat Lr34
against leaf rust and wheat Yr36 against wheat stripe rust. An array of
mechanisms for this type of resistance may exist depending on the
particular gene and plant-pathogen combination.
 Other reasons for effective plant immunity can include a lack
of coadaptation (the pathogen and/or plant lack multiple mechanisms
needed for colonization and growth within that host species), or a
particularly effective suite of pre-formed defenses

20.  The term GM is often used as a synonym of transgenic to refer to plants modified
using recombinant DNA technologies.
 Plants with transgenic/GM disease resistance against insect pests have been
extremely successful as commercial products.
 especially in maize and cotton, and are planted annually on over 20 million
hectares in over 20 countries worldwide.
 Transgenic plant disease resistance against microbial pathogens was first
demonstrated in 1986.
 Combining coat protein genes from three different viruses, scientists
developed hybrids with field-validated, multiviral resistance.
 Genetically or transgenic engineered disease resistance.

21.  A similar strategy was deployed to
combat papaya ringspot virus, which
by 1994 threatened to
destroy Hawaii’s papaya industry.
Field trials demonstrated excellent
efficacy and high fruit quality. By
1998 the first transgenic virus-
resistant papaya was approved for
sale. Disease resistance has been
durable for over 15 years. Transgenic
papaya accounts for ~85% of
Hawaiian production. The fruit is
approved for sale in the U.S., Canada
and Japan.

22.  Quantitative resistance
 Resistance, like other traits, occurs in a qualitative or in a quantitative way. With
the former the different genotypes in a population occur as discernible
phenotypes; it is usually controlled by a major gene.
 Quantitative resistance (QR) is defined as a resistance that varies in a continuous
way between the various phenotypes of the host population, from almost
imperceptible (only a slight reduction in the growth of the pathogen) to quite
strong (little growth of the pathogen).
 This resistance is often indicated with other terms such as partial, residual and field
resistance or even (wrongly) with tolerance. QR occurs at various levels to nearly
all important pathogens in most cultivars of our crops.

23.  DURABLE RESISTANCE
 Resistance is considered durable when it remains effective for a considerable
time, despite wide exposure.
 In this sense, it is a quantitative concept. The Rpg1 gene discussed above
was durable, but did not last forever.
And in the evolutionary sense, no resistance will last forever.
 It is possible to discern three groups of resistances that are predominantly
durable.
 QR against specialists and based on some to several genes with
additive effects seems durable.
 Resistance to pathogens with a wide host range.

24.  Non durable resistance
 In nature there is a constant race of arms between the attacking parasite and
the defending host, and in the evolutionary sense, all resistance is transitory.
 But large differences exist in the ease by which parasites can overcome a
resistance. In agriculture, too the durability of a resistance varies greatly.
 Resistance may already be neutralized in the last stages of the breeding
program (at zero years) and may, still be effective after more than 130 years
and wide exposure, as the case of the Phylloxera aphid resistance of grape.

25.  ACQUIRED RESISTANCE
 Some susceptible plants become systemically resistant in response to
localized infections, a phenomenon known as acquired resistance.
 This is best known in cucurbits and tobacco. When a lower leaf is infected,
the whole plant becomes resistant to the same and to other pathogens
and remains so for weeks.
 Plants with acquired resistance have high levels of pathogenesis - related
proteins, salicylic acid, peroxidase, and other factors (Scheffer, 1997).
 Obviously, there is a signalling mechanism that carries information to
distant parts of the plant, but the nature of the signals is unknown.

26.  Plant diseases cannot always be controlled by resistance. Resistance genes to
a specific pathogen may not be available in certain plants, or the suite of
quantitative resistance genes in some plants may not provide a sufficient level
of control.
 sometimes even where resistance is the primary means of controlling disease.
Some diseases can be avoided by growing crops in regions that are not
conducive to disease development. For example, many vegetable crops
grown for seed are produced in arid regions of the western US, where low
rainfall and a lack of extended leaf wetness necessary for infection inhibits
foliar and seed pathogens.
 Plant pathogens may be excluded during a growing season by using
pathogen-free seed or propagative parts. Heat treatment and meristem tip
culturing are used to rid plants of viruses and hot water treatments can
disinfest seeds of surface contaminating bacterial pathogens.
 Other Disease Control Strategies

27. Much progress has been made in understanding the molecular evolution of
plants and pathogens, and the integration of this information into crop
improvement programs or for disease management is ensuring sustainable crop
production for the immediate future. Still, the functions for very few pathogen
effectors are known, and often these are only in model systems. Our knowledge
is limited on how plant defense responses are differentially regulated or
modulated in the spectrum from PTI to ETI, and how this regulation can be
manipulated for better disease control. As an example, the relevance of
epigenetic controls on plant disease.

28.  https://pdfs.semantic scholar.org
 H Leung, International Rice Research Institute,
DAPO, Metro Manila, Philippines
 Plant Pathology, Fifth Edition
Textbook by George N Agrios.
 Wikipedia.
 https://www.britannica.com/science/pla
nt-disease.
 http://www.scielo.br/scielo.org
Reference

29. Thank you….