The document explores plant-pathogen interactions, detailing the molecular mechanisms of infection by fungi and bacteria, which manifest in various plant diseases. It introduces the gene-for-gene hypothesis by Harold Henry Flor, explaining genetic interactions between hosts and pathogens, and highlights the role of mechanical and chemical factors employed by pathogens to overcome plant defenses. Additionally, it discusses the impact of environmental factors on disease development and provides insights into programmed cell death and hypersensitive responses in plants.

1. Plant-pathogen Interaction and
Disease Development; Molecular
Mechanisms of Fungal and
Bacterial Infection in Plants;
Changes in Metabolism

2. Diseases ?
• Plant diseases are the result of infection by any
living organisms that adversely affect the growth,
development, physiological functioning and
productivity of a plant, manifesting outwardly as
visible symptoms.
• Any Parasite organisms that cause disease are
called pathogens and pathogens on parasitoid is
known as host.

3. Plant – Pathogen Interaction
• Plants exist in a world filled with bacteria,
fungi, nematodes, and possibly parasitic
plants (stariga, casccuta, orobaincy etc).
• They may be inoculated with viruses during
feeding by insects or by other vectors
(insects/pest, water, air, humans etc).
• Plant pathogens have made many adaptations
to enable them to invade plants, overcome
plant defense mechanisms, and colonize plant
tissues for growth, survival, and reproduction.

4. • Pathogens accomplish these activities
mostly through secretions of chemical
substances that affect certain components
or metabolic mechanisms of their hosts.
• Penetration and invasion, however, seem to
be aided by or in some cases be entirely the
result of, the mechanical force exerted by
certain pathogens on the cell walls of the
plant.
Plant – Pathogen Interaction

5. Harold Henry Flor, 1900–1991
• Flor received a Ph.D. degree in 1929 from
the University of Minnesota. He worked
for the USDA for three years at
Washington State University and then for
the remainder of his career at North
Dakota State University.
 In the 1940s, Flor developed the gene-for-gene
concept to explain the genetic interactions between
Melampsora lini and flax. His theories were put to
use in Flor’s own flax breeding program to
successfully develop rust-resistant flax. This concept
provided the underpinnings for research on the
genetics of host-pathogen interactions for the next
70 years.

6. Gene For Gene Hypothesis
• The concept of gene for gene hypothesis was first developed by Flor in
1956 based on his studies of host pathogen interaction in flax, for rust
caused by Malampsora lini.
• The gene for gene hypothesis states that for each gene controlling
resistance in the host, there is corresponding gene controlling
pathogenicity in the pathogen. The resistance of host is governed by
dominant genes and virulence of pathogen by recessive genes. The
genotype of host and pathogen determine the disease reaction.
• When genes in host and pathogen match for all loci, then only the host
will show susceptible reaction. If some gene loci remain unmatched, the
host will show resistant reaction. The gene for gene hypothesis is also
known as “Flor Hypothesis.”
• At molecular level, it is considered that gene for gene resistance usually
involves production of toxins antibiotic proteins by a resistance gene. The
production of toxins is related to gene dosage.
• The resistance controlled by domain gene is the most desirable. Gene for
gene relationship are rare or unknown for disease caused by viruses,
bacteria, Fusarium.

8. Biochemistry of Gene-for-Gene Hypothesis
• The Receptor-Elicitor Model of gene-for-gene interactions.
• The resistance allele of the plant encodes a receptor that
recognizes an elicitor produced by the pathogen. Recognition
of the pathogen elicitor by the plant receptor initiates plant
defense responses that lead to plant resistance.
• If the pathogen produces the elicitor, it is avirulent.
• If the pathogen does not produce the elicitor, it is virulent

9. Mode of Infection
 Virus
 Bacteria
 Fungi

10. (A) Mechanical Forces Exerted
on Host Tissues by Pathogens
• Viruses are usually introduced directly through the plant
cells by insects (BPH, WF, Aphids), Natural openings
(stomata), wounding site, therefore they do not exert
mechanical forces to inter in the host.
• Many fungi are known to apply mechanical forces on the
plant they are about to attack. When fungal spores lands
on a plant surface, and contact is established, diameter of
the tip of the hypha or radical in contact with the host
increases and forms the flattened, bulb-like structure called
the Appressorium.
• This increases the area of adherence between the two
organisms and securely fastens the pathogen to the plant.
From the appressorium, a fine growing point, called the
Penetration Peg arises and advances into and through the
cuticle and the cell wall.

11. (B) Chemical Weapons of Pathogens
• Some pathogens in plant are largely chemical in
nature. Therefore, the effects caused by pathogens
on plants are almost entirely the result of
biochemical reactions taking place between
substances (Hydrolytic enzymes) secreted by the
pathogen and those present in or produced by the
plant.
• The main groups of substances secreted by
pathogens in plants that seem to be involved in
production of disease either directly or indirectly,
are enzymes, toxins, growth regulators and
polysaccharides (plugging substances).

12. • Toxins seem to act directly on protoplast
components and interfere with the
permeability of its membrane and with its
functions. Growth regulators exert a
hormonal effect on the cells and their
increase or decrease their ability to divide
and enlarge.
• Polysaccharides seem to play a role only in
the vascular diseases, in which they
interfere passively with the translocation of
water in the plants.
(B) CHEMICAL WEAPONS OF PATHOGENS

13. (I) ENZYMES
(A) Cutinases:
• Cutin is the main component of the cuticle. The upper
part of the cuticle is admixed with waxes, whereas its
lower part in the region where it merges into the outer
walls of epidermal cells, is admixed with pectin and
cellulose.
• Cutinases break down cutin molecules and release
monomers as well as oligomers of the component fatty
acid derivatives from the insoluble cutin polymer e.g.
Fusarium spp. and Botrytis cinerea.

14. (B) Pectinases:
• Pectin substances constitute the main components of
the middle lamella i.e. the intercellular cement that
holds in place the cells of plant tissues. Several
enzymes degrade pectic substances and are known as
pectinases or pectolylic enzymes.
• 1. Pectic enzymes is pectin methyl-esterases, which
removes small branches off the pectin chains.
• 2. Pectic enzymes is a chain splitting pectinases called
polygalacturonases. It split the pectic chain by adding
a molecule of water and breaking the linkage between
two galacturonan molecules.
• 3. Pectin lyases is split the chain by removing a
molecule of water from the linkage, there by breaking it
and releasing products with an unsaturated double
bond. Examples of pathogens include Ralstonia
solanacearum, Didymella bryoniae.

15. (C) Cellulases:
• Cellulose is also a polysaccharide, but it
consists of chains of glucose (1-4) β-D-glucan
molecules. Saprophytes fungi, mainly certain
groups of basidiomycetes, and to a lesser
degree, saprophytic bacteria cause the
breakdown of most of the cellulose
decomposed in nature.
• In living plant tissues, however, cellulolytic
enzymes secreted by pathogens play a role in
the softening and disintegration of cell wall
material.

16. (II) MICROBIAL TOXINS
• Toxins are metabolites that are produced by invading
microorganisms and act directly on living host
protoplast, seriously damaging or killing the cells of
the plant.
• Some toxins act as a general protoplasmic poisons
and affect many species of plant representing
different families. Others are toxic to only a few plant
species or varieties and are completely harmless to
others. Many toxins exist in multiple forms that have
different potency.
• (A) Non-host specific toxin
• (B) Host specific toxin

17. • (1) Tab-toxin:-
its produced by the bacterium Pseudomonas syringae pv tabaci
which causes the wildfire disease of tobacco, by strain of pv tabaci
occurring on other hosts such as bean and soybean and by other
pathovars of P. syringae such as those occurring on oats maize and
coffee.
• (2) Phaseolo-toxin:-
its produced by the bacterium Pseudomonas syringae pv
phaseolicola, the cause of halo blight of bean and some other
legumes.
• (3) Ten-toxin:-
its produced by the fungus Alternaria alternata which causes
spots and chlorosis in plants by many species.
• (4) Cercosporin-
its produced by the fungus Cercospora and by several other fungi. It
causes damaging leaf spot and blight diseases of many crop plants
such as Cercospora leaf spot of Zinnia and gray leaf spot of corn.
(A) Non-Host Specific Toxin Or
Non Host-selective Toxins

18. (B) Host Specific Or Host-selective Toxins
1. Victorin or HV toxin – Its produced by the fungus
Cochliobolus Victoriae. This fungus infects the
basal portions of susceptible oat plants and
produces a toxin that is carried to the leaves, causes
a leaf blight and destroys the entire plant.
2. T-toxin- is produced by race T of Cochliobolus
heterostrophus, the cause of southern corn leaf
blight. Race T is indistinguishable from other all
other C. heterostrophus races except for its ability to
produce the T toxin.
3. HC-toxin- Its produced by Race 1 of C. carbonum
causing northern leaf spot and ear rot disease in
maize.

19. (iii) Growth Regulators
(a)Auxins-
• It occurs naturally in plants as indole-3-acetic acid
(IAA). Increased IAA levels occur in many plants
infected by fungi, bacteria, viruses, nematodes and
mollicutes, although some pathogens seem to lower
the auxin level of the host e.g Exobasidium azalea
causing azalea and flower gall, Ustilago maydis
causative organism of corn smut.
(b) Cytokinins-
Cytokinin activity increases in clubroot galls, in smut
and rust infected bean leaves. it is partly responsible
for several bacterial galls of leafy gall disease of sweet
pea caused by bacterium Rhodococus fasciens.

20. (c) Gibberellins-
• High level of gibberellins due to foolish seedling
diseases of rice, in which rice seedlings infected
with the fungus Gibberella fujikuroi grow rapidly and
become much taller than healthy plants is
apparently the result, to a considerable extent at
least, of the gibberellins secreted by the pathogen.
(d) Ethylene –
• In the fruit of banana infected with Ralstonia
solanacearum, the ethylene content increases
proportionately with the (premature) yellowing of the
fruits, whereas no ethylene can be detected in the
healthy fruits.
(iii) Growth Regulators

21. (IV) Polysaccharides
• Fungi, bacteria, nematodes and possibly other
pathogens constantly release varying amounts of
mucilaginous substances that coat their bodies and
provide the interface between the outer surface of the
microorganism and its environment.
• The role of the slimy polysaccharides in plant disease
appears to be particularly important in wilt diseases
caused by pathogens that invade the vascular system
of the plant.
• Large polysaccharide molecules released by the
pathogen in the xylem may be sufficient to cause a
mechanical lockage of vascular bundles and thus
initiate wilting.

22. Disease Development
• The amount of disease that
develops in a plant community
is dependent on properties of
• The Host,
• The Pathogen and
• The Environment
• The environment can affect
both the susceptibility of the
host (e.g. by creating stress in
the plant) and the activity of
the pathogen (e.g. providing
moisture for spore
germination).

23. Disease Development

24. Factors of Disease Development

25. Pathogen Host Environment
 Presence of pathogen
 Pathogenicity
 Adaptability
 Dispersal efficiency
 Survival efficiency
 Reproductive fitness
 Susceptibility
 Growth stage & form
 Population density &
structure
 General health
 Temperature
 Rainfall / Dew
 Leaf wetness period
 Soil properties
 Wind
 Fire history
 Air pollution
 Herbicide damage
Factors of Disease Development

26. Molecular Mechanisms of Fungal
Pathogenicity to Plants
1. Entry
• Fungi rarely cause disease in healthy immunocompetent hosts. Disease results
when fungi accidentally penetrate host barriers or when immunologic defects or
other debilitating conditions exist that favor fungal entry and growth.
2. Adaptation and Propagation
• Fungi often develop both virulence mechanisms (e.g., capsule and ability to grow
at 37oC) and morphologic forms (e.g., yeasts, hyphae, spherules, and sclerotic
bodies) that facilitate their multiplication within the host.
3. Dissemination
• Dissemination of fungi in the body indicates a breach or deficiency of host
defenses (e.g., endocrinopathies and immune disorders).
4. Host Factors
• Healthy, immunologically-competent individuals have a high degree of innate
resistance to fungi. Resistance to fungi is based primarily upon cutaneous and
mucosal physical barriers. Severity of disease depends on factors such as
inoculum, magnitude of tissue destruction, ability of fungus to multiply in the
tissue, and the immune status of the host.
5. Fungal Factors
• Enzymes such as keratinase, the presence of capsule in Cryptococcus
neoformans, the ability to grow at 37°C, dimorphism, and other as yet undefined
factors contribute to fungal pathogenesis which involves a complex interplay of
many fungal and host factors.

27. • The hyphae composed of protein polypepetides,
polysaccharide carbohydrates, fibrinogen or fibrin
and polynucleotides that contain RNA and DNA
material. This structure is bound together with
lignands that have stickiness properties.

28. • The cell wall of candida is composed of fibrin and the
plant fiber chitin or cellulose, mannoprotein-1, glucan
and mannoprotein-2, which are plant
polysaccharrides. Then comes a plasma membrane
and a protein nucleus. These components are
basically what candida uses to build the biofilm as
well.
• Candidase is a very strong enzyme for candida yeast
that eats the cellulose layers of the biofilm and cell
wall and the protein of the nucleus. But there are no
enzymes to eat the fibrin or plant polysaccharides.
• Candizyme is more complete than the above three
candida eating enzyme formulas. It contains enzymes
to eat the chitin/cellulose and the plant
polysaccharrides in both the biofilm and cell wall. It
also has protease enzymes to eat the protein of the
nucleus. However, like the rest it does not have an
enzyme that eats the fibrin in the biofilm.

29. First, bacterial nodulation (nod) genes are activated in response to
plant-secreted signal molecules such as flavonoids, resulting in
biosynthesis and secretion of lipo-chito-oligosaccharides (LCOs) by
rhizobium bacteria.
In the second step, LCOs elicit nodule formation on the host plant
roots and trigger the infection process. LCOs, which induce the
formation of the root nodules on the host plants, are termed Nod
factors.
Molecular Mechanisms of Bacterial
Pathogenicity to Plants

31. Changes in Plant Metabolism After Infection

32. Programmed Cell Death
• Programmed cell
death is a
genetically
regulated process of
cell suicide that is
central to the
development,
homeostasis and
integrity of
multicellular
organisms

33. NECROSIS VS APOPTOSIS

34. Purpose of Cell Death
• Cells that are produced in excess
• Cell that have no function
• Cell that develop improperly
• Cell that have stop further infection
• Cells that are harmful

35. Hypersensitive Response
• Rapid, localized plant cell death upon contact with
avirulent pathogens. HR is considered to be a key
component of multifaceted plant defense responses to
restrict attempted infection by avirulent pathogens
• Rapid - within 24 h
• Not always needed for resistance
• HR also contributes to the establishment of the long-
lasting systemic acquired resistance against
subsequent attack by a broad range of normally
virulent pathogens

36. • HR Includes:
• Oxidative bust (production of
reactive oxygen species)
• Disruption of cell membranes
• opening of ion channels
• Cross linking of phenolics
with cell wall component
• Production of anti-microbial
phytoalexins and PR protein
• apoptosis (programmed cell
death)

37. • A type III secretion pathway, broadly conserved among gram-negative
pathogens of plants and animals
• Macromolecular structure, Hrp pilus, acts as conduit for traffic (called
needle complex in animal pathogens)
• Encoded by clustered hrp genes
• Required for hypersensitive reaction and pathogenicity
• Expression induced in plant and in defined minimal media
• Capable of delivering proteins into host cells
• Secretes and delivers “effector proteins”
a) virulence factors
b) avirulence factors
The Hrp pathway

38. • Pectic enzymes
- Soft rot Erwinia spp.
- Multiple isozymes, some plant regulated
• Toxins
- e.g., coronatine acts as JA mimic to down regulate plant defense
• Extracellular polysaccharides
- Important in many diseases, specially vascular diseases
- Postulated roles in protection from plant-derived antimicrobials, osmotic stress,
dessication; evading recognition; causing wilt, etc.
• Quorum sensing (cell-cell signaling) and global regulation
of virulence
- Soft rot Erwinia spp. regulation of virulence associated genes, including pectic
enzymes
- Cell wall degradation products elicit plant defense, so benefit to repressing pectolytic
activity until high numbers of bacteria accumulate.
• The Type III secretion (Hrp) pathway
- Essential for necrogenic Gram negative pathogens
Major changes after Infection of Erwinia spp.

39. K K
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