1 PHYSIOLOGY OF HOST-PARASITE INTERACTION 1. FUNGAL CLASSIFICATION :TROPHIC SYSTEM 2....
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PHYSIOLOGY OF HOST-PARASITE INTERACTION
1. FUNGAL CLASSIFICATION :TROPHIC SYSTEM
2. HISTOPATHOLOGICAL AND ULTRASTRUCTURAL OF PATHOGENESIS
3. BIOCHEMICAL OF PATHOGENESIS:
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ENZYME AND TOXIN OF COCHLIOBOLUS
INFECTION
Trophic system:
1. Mutualistic Symbiont
2. Biotroph3. Hemibiotroph
4. Necrotroph
5. Saprotroph
Degree of specialization:
High
Low
More physiological synchronization between host-pathogen
- Cause minimum effect to their host and inceasedependence to living host cell
- Less dependence to wall degrading enzyme and toxin- Selective and site specific use of enzyme- Selective of involvement of phytohormone- Restricted host range- Synchronize physiological process of host-pathogen
- Cause extensive damage to the host by degradingenzyme > secondary toxic metabolites
- More dependence to the host- Less saprophytic ability
1.FUNGAL CLASSIFICATION :TROPHIC SYSTEM
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1. HISTOPATOLOGICAL AND ULTRASTUCTURAL OF PATHOGENESIS
Cladosporium fulvum:
- Caused leaf spot (necrotic) of tomato- Attach to the leaf by extracellular protein (EP)
- Infection on lower surface of the leave, plant response towards avirulent andvirulent strain, differ
- Conidia germinate to form runner hyphae (2-3 um) until open stomata found,penetrate (3-5 days after inoculation), hyphae enlarge (4-5um), grow intercellularly
- penetration peg
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HR
- Hyphae in close contact to mesophyll, do not form haustoria and no defenseresponse on succeptible cultivar
- After penetration, fungal growth arrested, hypersensitive (HR) defense reaction onresistant cultivar , mesophyll cells accumulates substance
- Within 2 weeks conidia were formed on the lesion on succeptible, but not onresistant cultivar
basic compatibilty
specific-racecompatibility
COMPATIBILITY
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produce glycoprotein,non specific elicitor
• Induce necrosis in tomato leaves• Not race specific
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Produce and accumulate phytoalexinElectrolyte leakageIncrease lipoxygenaseIncrease lipoperoksidase
2. BIOCHEMICAL OF INTERACTION
A. Extracellular substanse, non specific elicitorCladosporium fulvum
Hypesensitive reaction
• Helminthosporoside Cohliobolus sacchari, pathogen of sugarcane
1 of 3 isomer of sesquiterpenoids binds to 1-4 galactofuranose by linkage
- if contain less than 4 galactose unit inactive or protect sugarcane against HS-toxin- B. Sacchari, anamorph, produce galactofuranosidase that remove galactose from HS-
toxin
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• HV-toxin (Victorin) C. victoriae on oat var. victoria----- blight• T-toxin• HC-toxin
C. heterosporus race T on maize Texas male sterile cytoplasm (Tcms)C. carbonum race 1 on maize (inbread line) ------ blight
Do not play a major role in host-parasite interaction
B. ENZYME AND TOXINCOCHLIOBOLUS
1. Enzyme:- CWDEs:
a. endoplygalacturonase and endo-xylanase, toxic and induce phytoalexin accumulationb. Cellulose, pectinase, endo=polygalacturonase degrading enzyme
2. HS (Host selective)- Toxin:
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C. INFECTION
a. PENETRATION OF CUTICLE
b. ENTRY THROUGH CELL WALL
c. PLANT DEFENCE: - DETOXIFICATION OF PHYTOALEXIN
- PRODUCTION OF ANTI-FUNGAL PROTEIN
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a. CUTICULAR PENETRATION
Penetration by:Physical force with assistance of degrading enzyme
Enzymatic degradation:Germinating spore (tips of germ tube) F. Solani f.sp pisi produce
cutinase: depolymerize cutin
Diisopropylfluorophosphate (DFP)N-butylisocyanate (benomyl)Organophosphoric fungiside ( serine inhibitors, 6-chloro-2-pyrone
derivates)
cuticle rupture
cutinase inhibitor,prevent cuticle rupture
no infection
Cutinase: inducible enzyme• Ability to degrade cutin (production of cutinase) ----------- degree of virulence• Rupture cuticle -------------------- not induce cutinase production• Avirulent isolate ----------low cutinase producer-------penetrate through stomata or wound
Cutinase gene expression:• Virulence isolate : multicopy of cutinase gene• Avirulent isolate : single copy of cutinase gene• Spores of highly virulent strain have cutinase but not sufficient for infection,
for cutin surface recognition
• Contact with cutin-------------- induce cutinase production synthesis• Transcription ------------------- 15 min after contact with cutin
• Cutin monomers (hydroxy acids) ----------- true inducers ----------- plant suceptibility
Transcription:Cutinase gene ------ 135 bp, four promoter and a silencer, a positive acting G-rich element
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b. Entry
Fungi
through cell wall
produce endo and exopectinase, and endopectate lyase
degrade
Pectin: major cell wall component
Self catabolite repression
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demetylate
Less inhibitory product
- Detoxification of phytoalexin
Pea phytoalexin:- pisatin (isoflavonoid compound)- absent in healthy plant- accumulate, 5% dry weight, a few days after infection F. solani fsp. pisi
(N. Haematococca)
P40 cytochrome demethylasePisatininduce
repress
glucose
VirulenceHigh, tolerate , demethylate pisatinLow, sensitive , could not demetylate pisatin
Gene control pisatin production: P da gene, meiotic instable
May be lost
c. Plant defence
1. Reinforcing cell wall to limit ingress of pathogens: production ofphenolic substance
2. Producing antifungal protein3. Producing phytoalexin:
- a low molecular weight toxic compound to fungi- synthesize and accumulate at the site of infection after exposure to
pathogen
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- Production of anti-fungal protein
Plant pathogen or pathogen elicitors
Altered protein synthesis , including anti-fungal protein2 chitinase and 2 1,3 glucanase
Degrade or inhibit fungal pathogen degrade chitin degrade glucan
Fungal cell wall
Glycosidic fragment
Chitosan, hexosamine fragment
Pisatin production in plant Inhibits fungal growth
3. MATING TYPE AND PATHOGENESISINFECTION
• Important for smut as fusion ofhaploid cells of opposite matingtype is prerequisite for infection
• Dikaryotic hyphae developed inhost tissue
• Promycelium may infect hostdirectly
• Mat locus of U. maydis (a1 and a2formed pheromone andpheromone receptors)
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