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BASIC OF PHYTOPATHOLOGY
3. LECTURE
PLANT-PATHOGEN INTERACTION
© 2012 A. Lebeda, B. Mieslerová, M. Sedlářová
PHYTOPATHOLOGY
3. LECTURE – PLANT-PATHOGEN INTERACTION
Syllabus :
1. Classification and characterization of biotic interactions
between organisms
2. Parasitism of plant pathogenic microorganisms; forms of
parasitism
3. Pathogenism, its classification, pathogenicity and its
determinants
4. The specificity of the interaction between the host and the
pathogen, the level of specificity, mechanisms determining the
specificity of the plant- pathogen interaction
5. Evolution of parasitism and pathogenism
CLASSIFICATION OF
SYMBIOTIC INTERACTIONS
MUTUALISM - symbiotic interaction
between different species that is
mutually beneficial
COMMENSALISM - relationships
between two organisms where one
organism benefits from the other
without affecting it
PARASITISM - a non-mutual relationship
between species, where one species,
the parasite, benefits at the expense of
the other, the host
BIOTROPHIC PARASITES – parasites that need living cells
NECROTROPHIC PARASITES - parasites that kill host, then feed on the dead matter
MODEL OF RELATIONSHIPS BETWEEN THE THREE MODES
OF FUNGAL NUTRITION
Biotrophs – fungi
must obtain nutrition
from living material
(plant, animal)
Necrotrophs - fungi
occur on living
material, but must kill
part of tissue for
obtaining nutrition
(toxins)
Saprotrophs - fungi
living on dead
material
LIVING STRATEGY OF PARASITES
OBLIGATE BIOTROPHY
Common features:
• Intracellular penetration by cells or haustoria
• Invagination of plasmalemma and following
perforation
• Ektoparasites (Erysiphales), endoparasites
(Peronosporales)
• Hypersensitivity
• Host nucleus is living
• Host specialisation
Puccinia graminis
• Complicated or impossible cultivation in
axenic culture
Examples: Plasmodiophora brassicae
(Plasmodiophoromycota), Synchytrium
endobioticum (Chytridiomycota), Peronosporales
(Oomycota),
Erysiphales,
Taphrinales (Ascomycotina),
Uredinales, Ustilaginales, Tilletiales
(Basidiomycotina)
Blumeria graminis
LIVING STRATEGY OF PARASITES
NECROTROPHY
• They attack and quickly kill living
cells, cause tissue maceration
• Produce enzymes, toxins
• Cause disruption of cell wall,
protoplast metabolism
• May exist as saprotroph
• Good cultivation on artificial
media
• Broad host range
OBLIGATE
Diseases of fruits, leaves, stems
and roots
Pythium, Armillaria, Sclerotinia,
Fusarium, Verticillium, Sclerotium
Sclerotinia
Fusarium
LIVING STRATEGY OF PARASITES
HEMIBIOTROPHY
• Form between necrotrophy and
biotrophy
• Cultivation in axenic culture
possible
• Highly reduced saprotrophic
existence
Examples: Venturia inaequalis,
Rhynchosporium secalis,
Phytophthora infestans
Venturia inaequalis,
Phytophthora infestans
LIVING STRATEGY OF PARASITES
FACULTATIVELY SAPROTROPHIC HEMIBIOTROPHY
•
•
•
•
Form between biotrophy, necrotrophy and saprotrophy
Cultivation in axenic culture possible
Highly specific parasites
Frequently occurring in 2 different forms: monokaryotic mycelium
(biotrophic) and dikaryotic mycelium (saprotrophic)
Crinipellis perniciosa
(Basidiomycota, obligate
parazite of cacao)
LIVING STRATEGY OF PARASITES
FACULTATIVELY SAPROTROPHIC BIOTROPHY or
BIOTROPHIC SAPROTROPHS
•
•
Ability of biotrophic and necrotrophic nutrition
Frequently linked with occurrence of two different forms of pathogen:
monokaryotic mycelium (saprotrofic phase) and dikaryotic mycelium
(biotrofic phase)
• Highly specific parasites
Examples:
Hemiascomycetes
Taphrinales (Ascomycota)
Taphrina deformans
LIVING STRATEGY OF PARASITES
FACULTATIVELY SAPROTROPHIC NECROTROPHS or
NECROTROPHIC SAPROTROPHS
• Ability of saprotrophic and necrotrophic nutrition
• In contact with living host plant they are changing for necrotrophy
• After depletion of nutrition, persistence on dead organic substrates,
• Broad spectrum of hosts, diseases of fruits and tubers
• No problems with cultivation in axenic culture
Examples : Aspergillus,
Penicillium, Botrytis (Ascomycota)
Rhizopus (Zygomycota)
Rhizoctonia (Basidiomycota)
Penicillium, Aspergillus
LIVING STRATEGY OF BIOTROPHS, HEMIBIOTROPHS
AND NECROTROPHS
PPG, plant pathogenicity-related gene; PMP, primary metabolism pathway; SMP,
secondary metabolism pathway; PCWDE, plant cell wall degrading enzyme; SP, spore;
AP, appressorium; HA, haustorium; BH, biotrophic hyphae; NH, necrotrophic hyphae;
SB, sclerotium-like body; MN, mycelial network.
LIVING STRATEGY OF PARASITES
GENETICAL PARASITISM
•
•
•
•
Genetic colonization
Parasite incorporates portion of its DNA into the host genome
Agrobacterium tumefaciens, A. rhizogenes
The Ti-plasmid (tumor-inducing), part of the T-DNA of plasmid transfer
into the host genome - tumor - opines that utilizes a power source
Agrobacterium tumefaciens
VECTORS CAPABLE OF TRANSFERRING GENETIC
MATERIAL
Šutić,
Sinclair
(1991)
EVOLUTION OF BIOTROPHY, NECROTROPHY AND
SAPROTROPHY
PATHOGEN VS. PARASITE
PATHOGEN = cellular organism
or virus able to cause disease in
a particular host
PATHOGENISMS
PARASITIC
NON-PARASITIC (exopathogenism –
e.g. Aflatoxines cause virescence of
corn seedlings)
PARASITE - organism or virus,
existing in close coexistence with
other organisms, from whose tissues
obtained substances necessary for
its nutrition - nutritional addiction
Phragmidium mucronatum
PATHOGENIC AND EPIDEMIC POTENTIAL OF
ORAGNISMS CAUSING INFECTIOUS DISEASES
• Defined range of host plants for each pathogen
• Development of classification systems, originally derived from
medicine
• DESCRIPTIVE TERMS
infectious unit, inoculum, local lesions
• MATHEMATICAL EXPRESSION (MEASURABLE TERMS)
airborne spore concentration, sporulation potential, inoculum
density, infection period, gradient of disease
Other uses:
Pathometry
Epidemiology
PATHOGENICITY
• The ability of pathogen / parasite interfere with one or more
essential functions of plants and can cause the pathological
process
• Qualitative (virulence) and a quantitative component
(aggressiveness)
• Robinson (1976) - division:
p. vertical (varietal specific)
p. horizontal (varietal nonspecific)
INVASIVITY
• The ability of the microorganism to penetrate host tissues, keep
them and reproduce
• Does not include the ability to cause disease symptoms
INFECTIVITY
• The ability to cause disease after penetration into the host
PATHOGENICITY AND CLASSIFICATION OF CRITERIA
THAT DEFINE IT
Criteria
Virulence
Aggressiveness
1. Taxonomic group –
species, subspecies
+
+
Strain
(+)
+
Pathovar
(+)
+
Forma specialis
+
(+)
Pathotype
+
(+)
Race
+
(+)
Biotype
+
3. Specificity of
interaction
Specifically differentiated Specifically
compatibility undifferentiated
incompatibility
compatibility incompatibility
4. Genetical background
Mono-, oligogenic
Polygenic
5. Epidemiology
Varietal specific
Varietal unspecific
6. General character
Quality, discontinuity
Quantity, continuity
2. Xenopatic group
Pathogenicity
VIRULENCE
•
Marking qualitative differences in pathogenicity
• The possibility of differentiating the interaction between isolates
(races) of pathogen and varieties (lines) of host
• Differences in virulence between isolates - discontinuous
characters
• Mostly in interactions of gene-for-gene
• Genetically fixed
• Oligogenic, usually
recessive
• The impact of environment
• Quantitative differences
•
(Sporulation intensity ...)
• Biotrophic parasites –
powdery mildews, downy
mildews, rusts
Pathogen
Host
Reaction of different genotypes of Cucumis melo to isolates
of cucumber powdery mildew (Golovinomyces orontii)
Pathogenicity
AGGRESSIVENESS
• Marking quantitative differences in pathogenicity of isolates
• No differentiation response, but the constant quantitative
overview
• Isolates can be sorted by continuous aggression
• Mostly specifically undifferentiated compatibility
• Varietal nonspecific resistance
• Polygenic +
•
cytoplasmic systems
• The impact of
environment fluctuation
• viruses, bacteria,
•
necrotrophic
mycoparasites
•
some biotrophs
Pathogen
Host
Susceptibility of
plant vs.
Aggressiveness of
pathogen
DETERMINANTS OF PATHOGENICITY
• Ability of pathogenic agents cause disease is affected by their
ability to:
• Penetrate into plants
• Catabolize substances of host, incorporated and used
• Reproduce itself
• Quickly paralyze the host defense mechanisms
Three types of pathogens:
1 / actively degrade the structural integrity of the host
2 / inhibit selective processes / host enzymes
3 / intervene in the regulatory systems of host
Determinants of pathogenicity - the means by which the pathogen is
equipped to penetrate into the host and induce disease
1. Physical agents and mechanical strength
2. Chemical agents
3. Distortion of biosynthesis by direct interaction with DNA
Determinants of pathogenicity
1. Physical agents and mechanical strength
Especially with fungal pathogens
Penetration
Invasion
Mycelial growth
Fructification
Disruption of the epidermis - water losses - Uredinales,
Albugo sp.
Covering assimilation area – powdery mildews
Growth vascular species - reduction of water transport Graphium
Penetration
•
•
•
•
Through stomata (rust)
Through trauma (e.g. Venturia, Sclerotinia fructigena)
Using young parts of tissues (root hairs)(Fusarium)
Direct penetration (powdery mildews, downy mildews)
Penetration of rust urediospore
through stoma
Different modes of
invasion and mycelial
growth of selected
pathogens
Determinants of pathogenicity
2. Chemical agents
2.1. Toxins
• Nonenzymatic organic substances in
low concentrations deleteriously
affecting normal processes in the
living organism
non specific
specific
• Production by necrotrophic
pathogens
Mechanisms of action - according to
specific substances:
• Cellular poisons (fusikokcin
Fusicoccum amygdalii –
hyperpolarisation of membranes)
• Inhibition of enzymes
• Inhibition of synthesis nucleid acids,
proteins, chlorophyll
Erwinia amylovora causing fire
• Metabolisms of phenols…
blight
Host-specific toxins produced by phytopathogenic fungi
Alternaria mali
Alternaria citri
Corynespora cassiicola
Drechslera maydis
Phoma tracheiphila
Host-specific toxins produced by phytopathogenic bacteria
Pseudomonas syringae pv.
lycopersici
The host-nonspecific toxins produced by phytopathogenic fungi
Fusarium spp,
production of
fusarium acid,
trichothecenes
(toxic to
herbivores,
and misused)
Penicillium patulum –
produces dangerous
toxin Patulin
Trichothecens
KIMURA, ANZAI, YAMAGUCHI (2001)
J. Gen. Appl. Microbiol. 47, 149–160
Determinants of pathogenicity
2. Chemical agents
2.2. Enzymes
Enzymatic degradation of the cell wall forming agents
Determinants of pathogenicity
2. Chemical agents
2.2. Enzymes - cutinase
Determinants of pathogenicity
2. Chemical agents
2.2. Enzymes - pectinase
Degradation of pectin
- Erwinia amylovora
- Botrytis, Fusarium, Monilia fruticola
Determinants of pathogeniicity
2. Chemical agents
2.2. Enzymes - cellulase
Determinants of pathogeniicity
2. Chemical agents
2.3. Phytohormones
Production of cytokinins, auxins,
gibberellins, ethylene,
brassinosteroids
1 / pathogen itself
2 / induction of endogenous levels
Changes in growth
• Hyperplasy
• Hypertrophy
e.g. Witches broom, tumors, deformation of
plant organs
Determinants of pathogeniicity
3. Direct interaction with the host DNA
• Viruses, viroids, plasmids
• Disruption of the function of chloroplasts
• Extra-chromosomal genetic determinants - plasmids, episomes
CLASSIFICATION OF PLANT-PATHOGEN RELATIONSHIPS
1. Interaction nonhost-nonpathogen:
not infectious microorganism
plant is immune
2. Interaction host-pathogen
both components are biologically compatible
A Compatible response:
after penetration into the host develops an
infection, pathogen reproduces
B Incompatible response:
after penetration into the host
infection is suppressed (HR or other
response) pathogen does not
reproduce
Diagram of the concept of basic incompatibility and
(Lebeda, 1984)
basic compatibility
Plant - microorganism
Preformed defense mechanisms; Initiation
of general defense reactions
Basic incompatibility
(nonhost - nonpathogen)
General metabolic and genetic
host defense mechanisms
(species)
Nespecifical
incompatibility compatibility
General defense mechanisms ineffective
Basic compatibility
(host- pathogen)
Highly specific metabolic and
genetic adaptation of host
(cultivar, line..)
Specificaly differentiated
incompatibilitycompatibility
Specific complex of metabolic
and genetic defense mechanisms
of host (cultivars etc.)
Specificaly nondifferentiated
incompatibility-compatibility
Compatibility – incompatibility
Gurr a Rushton (2005)
Model of interaction plant – fungal pathogen
Blumeria graminis
Gurr a
Rushton
(2005)
Comparison of vertical and horizontal resistance
Selection of resistance to the disease in plant
population
Race specific resistance
Race of microorganism
Host
genotype
Examples of the occurrence and distribution of race specific
resistance in natural pathosystems (Burdon et al., 1996)
Evolution of interaction gene-for-gene
in wild pathosystems
Linum marginale
– Melampsora lini
Coevolution of hostpathogen interaction
The response to infection and
the possible development or
suppression of manifestations
of the disease depends
primarily
on the genetic background of
both partners
proces
rozpoznání
Theory „gene-for-gene“
(Flor, 1946 resp. 1947)
Genes resistance (the host plant),
respectively genes avirulence (for a
pathogen) encode proteins
essential for recognition (cell
receptors, resp. elicitor molecule)
The validity of this assumption was
later confirmed by cloning the
avirulence genes of various
pathogens (Keen, 1990)
Michelmore a Meyers (1998)
Evolution of genes of virulence, resistance and avirulence
Evolution of virulence in Bremia lactucae population
on lettuce
Lebeda a Schwinn (1994)
Introduction of resistance to powdery mildew in barley
cultivars in the UK and the subsequent selection of
virulence genes in the Erysiphe population
Coevolution of host and pathogen:
„Boom and Bust“