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1 PHYSIOLOGY OF HOST-PARASITE INTERACTION 1. FUNGAL CLASSIFICATION :TROPHIC SYSTEM 2. HISTOPATHOLOGICAL AND ULTRASTRUCTURAL OF PATHOGENESIS 3. BIOCHEMICAL.

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Presentation on theme: "1 PHYSIOLOGY OF HOST-PARASITE INTERACTION 1. FUNGAL CLASSIFICATION :TROPHIC SYSTEM 2. HISTOPATHOLOGICAL AND ULTRASTRUCTURAL OF PATHOGENESIS 3. BIOCHEMICAL."— Presentation transcript:

1 1 PHYSIOLOGY OF HOST-PARASITE INTERACTION 1. FUNGAL CLASSIFICATION :TROPHIC SYSTEM 2. HISTOPATHOLOGICAL AND ULTRASTRUCTURAL OF PATHOGENESIS 3. BIOCHEMICAL OF PATHOGENESIS: ENZYME AND TOXIN OF COCHLIOBOLUS INFECTION Trophic system: 1. Mutualistic Symbiont 2. Biotroph 3. Hemibiotroph 4. Necrotroph 5. Saprotroph Degree of specialization: High Low More physiological synchronization between host- pathogen - Cause minimum effect to their host and incease dependence 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 degrading enzyme > secondary toxic metabolites - More dependence to the host - Less saprophytic ability 1.FUNGAL CLASSIFICATION :TROPHIC SYSTEM

2 2 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 and virulent 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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4 4 HR - Hyphae in close contact to mesophyll, do not form haustoria and no defense response on succeptible cultivar - After penetration, fungal growth arrested, hypersensitive (HR) defense reaction on resistant cultivar, mesophyll cells accumulates substance - Within 2 weeks conidia were formed on the lesion on succeptible, but not on resistant cultivar basic compatibilty specific-race compatibility COMPATIBILITY

5 produce glycoprotein, non specific elicitor Induce necrosis in tomato leaves Not race specific Produce and accumulate phytoalexin Electrolyte leakage Increase lipoxygenase Increase lipoperoksidase 2. BIOCHEMICAL OF INTERACTION A. Extracellular substanse, non specific elicitor Cladosporium fulvum Hypesensitive reaction HelminthosporosideCohliobolus 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 5 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 TOXIN COCHLIOBOLUS 1. Enzyme: - CWDEs: a. endoplygalacturonase and endo-xylanase, toxic and induce phytoalexin accumulation b. Cellulose, pectinase, endo=polygalacturonase degrading enzyme 2. HS (Host selective)- Toxin:

6 6 C. INFECTION a. PENETRATION OF CUTICLE b. ENTRY THROUGH CELL WALL c. PLANT DEFENCE: - DETOXIFICATION OF PHYTOALEXIN - PRODUCTION OF ANTI-FUNGAL PROTEIN

7 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 min after contact with cutin Cutin monomers (hydroxy acids) true inducers plant suceptibility Transcription: Cutinase gene bp, four promoter and a silencer, a positive acting G-rich element 7

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9 9 b. Entry Fungi through cell wall produce endo and exopectinase, and endopectate lyase degrade Pectin: major cell wall component Self catabolite repression

10 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) P 40 cytochrome demethylase Pisatin induce repress glucose Virulence High, tolerate, demethylate pisatin Low, 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 of phenolic substance 2. Producing antifungal protein 3. Producing phytoalexin: - a low molecular weight toxic compound to fungi - synthesize and accumulate at the site of infection after exposure to pathogen 10

11 - Production of anti-fungal protein Plantpathogen or pathogen elicitors Altered protein synthesis, including anti-fungal protein 2 chitinase and 2  1,3 glucanase Degrade or inhibit fungal pathogendegrade chitindegrade glucan Fungal cell wall Glycosidic fragment Chitosan, hexosamine fragment Pisatin production in plantInhibits fungal growth 3. MATING TYPE AND PATHOGENESIS INFECTION Important for smut as fusion of haploid cells of opposite mating type is prerequisite for infection Dikaryotic hyphae developed in host tissue Promycelium may infect host directly Mat locus of U. maydis (a1 and a2 formed pheromone and pheromone receptors) 11


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