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PLANT STRESS RESPONSE STRESS • Manifold unfavourable, but not necessarily immediately lethal conditions, occurring either permanently or sporadically in a locality • Significant deviation from optimal conditions for life • Elicit responses and changes at all functional levels of the organism • May be first reversible, but may become permanent STRESS • Conditions that adversely affect growth, development, productivity 1. Abiotic (phy/che environment) 2. Biotic (organisms) • Abiotic- water logging, drought, high or low temperatures, excessive soil salinity, inadequate mineral nutrients, too much or too little light, ozone RESISTANCE • Depends on 1. Species 2. Genotype 3. Age of plant 4. Tissue identity 5. Duration, severity, rate of stress 1. 2. 3. 4. 5. 6. 7. Alarm phase – stress reaction Restitution- repair Hardening Adjustment Adaptation- normalization (Exhaustion)- irreversible damage End phase STRESS RESPONSE • Race b/w effort to adapt and potentially lethal processes in protoplasm • Triggered by stress or stress- induced injury (membrane integrity loss) • Some- enable plant to acclimatize to stress • Altered gene expression- changes in development, metabolism • Initiated when plant recognizes stress at cellular level- proteins that sense abiotic stress • Transmit information within individual cells and through out the plant • increase in specific mRNA, enhanced translation, stabilization of proteins, alteration of protein activity WATER DEFICIT • Major a biotic stress • Induced by many environmental conditions: 1. No rainfall- drought 2. High salt conc. 3. Low temp. 4. Transient loss of turgor at midday • Rate of onset, duration, acclimatizationinfluence the water stress response Response to water deficit • ABA phytohormone • Induce expression of drought- inducible genes • Products- 2 groups A. GROUP 1 1. Protective proteins 2. Water channel proteins, membrane transporters 3. Osmoregulator synthesizing enzymes 4. Detoxifying enzymes (peroxidases, catalases) B) GROUP 2 1. Transcription factors (DREB, MYC) 2. Protein kinases (MAP kinases, CDP kinases) 3. Proteinases (phospholipase) • 4 independent pathways 1) 2 - ABA-dependent 2) 2 - ABA- independent • Cis acting elements- in promoter of all stress inducible genesABA-responsive element (ABRE) dehydration responsive element (DREB) COLD- STRESS • Plants produce a no. of proteins in response to cold and freezing temp. • 54 cold inducible genes • 10% of drought induced genes- also induced by cold • Genes- contain a cis element repeat (CRT)- 5 bp seq. • Transcription factor- C repeat binding factor (CBF)- Main controlling switch in monocots, dicots Cold stress reactions • Injury to cell membrane – chilling, freezing • Ratio of saturated to unsaturated fatty acidsdegree of tolerance, particularly in plastids • Non- acclimatized plants- killed or injured at 100 C or below. • Freeze acclimatized trees- survive between 40 to -500C • Injury- by severe dehydration during freezethaw cycles • Temp below 00C , cellular water freeze. • Cell shrinkage • Expansion induced lysis • SURVIVAL STRATEGIES: anti freeze proteins (AFP) - Declines rate of ice crystal growth - Lowers the efficiency of ice nucleation sites - Lowers temp. at which ice forms Osmoprotectants - osmolytes- quarternary amines, amino acids, sugar alcohols - Balances the osmotic potential of externally increased osmotic pressure • Glycine betaine • Quaternary amine, soluble • CH3 gps- interact with hydrophobic and hydrophilic molecules • Oxidationcholine (choline monooxygenase)> betaine aldehyde • Betaine aldehyde (betaine aldehyde dehydrogenase)> glycine betaine • Proline • Sugar alcohols –mannitol • Trehalose- non reducing disaccharide • Increased water retention and desiccation tolerance SALT STRESS • Flow of water is reversed- imbalance • Accumulation of excess Na+, Cl- in cytosol • Stress tolerant plants- maintains internal osmotic pressure Sensing salt stress • Ion specific signals of salt stress • High Na+- increases Ca2+ conc. In cytoplasmKey component of Na+ signalling • SOS3 – Ca2+ binding protein • Activates protein kinase (SOS2) • Phosphorylates (activates) plasma membrane H+-Na+ antiporter (SOS1) • SOS1 mRNA- stabilized, accumulates • Plant maintains high K+, low Na+ in cytosol • 3 tolerance mechanisms1) Reducing Na+ entry to cells 2) Na+ efflux from cell (K+-Na+) 3) Active transport to vacuole (vacuolar H+-Na+ ATPase) Na+ sequestration • In vacuoles • By NHX1, NHX2 proteins of tonoplast membrane • Decreases cytoplasmic Na+ Salt stress induced proteins • Transcription of genes oncoding late embryogenesis abundant (LEA) proteinsactivated Antioxidant production • Abiotic stress – drought, salt, chill- increases reactive O intermediates (ROI) in plants • ROI- stress signal- due to altered metabolic functions of chloroplast, mitochondria ROI SCAVENGING Antioxidant system contains a battery of enzymes that scavenge ROI- SOD, peroxidases, catalases, glutathione reductases HEAT STRESS • • • • • • • Decrease in synthesize of normal proteins Transcription and translation of HSPs When 5o C rise in optimum temp. Conserved proteins Act as chaperons, refolding classes- based on mw Hsp 100, Hsp 90, Hsp 70, Hsp60 FLOODING -Decreases O2 availability of plant roots -ATP production is lowered -SURVIVAL STRATEGIES: production of enzymes for sucrose, starch degradation, glycolysis, ethanol fermentation -ethylene- long term acclimatization responsesstem elongation BIOTIC STRESSES INDUCED STRUCTURAL AND BIOCHEMICAL DEFENCES • Plants receive signal molecules as soon as pathogen contact • Elicitors of recognition • Host receptors – on plasma membrane or cytoplasm • Bichemical reactions, structural changes – to fend off pathogen, toxins Signal transduction • Transmission of alarm signal to host defense providers • To host proteins, nucleur genes- activatedproducts that inhibit pathogen • Signals to adjacent cells, usually systematically • Intracellular signal transducers- protein kinases, Ca2+ ,phosphorylases, phospholipases, ATPases, H2O2,ethylene. • Systemic signal transduction, aquired resistance- by salicylic acid, oligogalacturonides from plant cell walls, jasmonic acid, systemin, fatty acids, ethylene Induced structural defenses • After pathogen has penetrated preformed defense structures- plant respond by one or more structures to prevent further pathogen invasion • Defense structures: 1) cytoplasmic defense reaction 2) cell wall defense structures 3) histological dfense structures 4) necrotic/ hypersensitive defense reaction Cytoplasmic defense reaction • In response to weakly pathogenic and mycorrhizal fungi • Induce chronic diseases / nearly symbiotic conditions • Cytoplasm surrounds hyphal clump • Cytoplasm and nucleus enlarge • Dense granular cytoplasm • Mycelium disintegrates, invasion stops. Cell wall defense structures • Morphological changes of cell wall • Limited effectiveness • a) parenchymatous cells’ walls swell, produces amorphous, fibrillar material that surrounds, traps bacteria • b) cell wall thickens by a cellulosic material infused with phenolics • c) callose papillae laid of inner surface of cell wall (2-3 mins ) (fungi) formation of lignituber around fungal hyphae Histological defense structures • Formation of cork layers- fungi, bacteria, virus, nematodes inhibits invasion beyond initial lesion prevents flow of nutrients • Abscission layers- fungi, bacteria, virus gap b/w 2 circular cell layers surrounding infection site • Tyloses- over growth of protoplasts of adjacent parenchymatous cells- protrude into xylem vessels through piths • Gums- around lesions intracellular spaces, within surr. cells. ABSCISSION LAYER TYLOSE FORMATION Necrotic defense reaction • • • • • Hypersensitive response Brown resin-like granules in cytoplasm Browning continues, cell dies Invading hypha- degenerates Bacterial infections- destruction of cell membranes, desiccation, necrosis of tissue • Obligate parasites- fungi, bacteria, nematode, viruses INDUCED BIOCHEMICAL DEFENSES • • • • • • HYPERSENSITIVE RESPONSE(HR) Initiated by elicitor recognition Rapid burst of oxidative reactions ↑sed ion movement (H+, K+) Loss of cellular compartmentalization Crosslinking of phenolics with cell wall Production of antimicrobials HR • due to plant R (resistance) gene • Pathogen produced elicitor- from its Avirulence gene • Eg:- arv D gene of P. syringae- enzyme involved in synthesis of syringolides (hypersensitive response in soya bean) • Eg:- protein of tobacco R gene- protect against leaf spotting bacterium – in cytoplasm • Eg:- protein of Cf9 R gene of tomato- against race 9 of leaf mould fungus- outside plasma membrane ACTIVE O RADICALS, LIPOXYGENASES, CELL MEMBRANE DISRUPTION • Pathogen attack, exposure to toxins, enzymespermeability changes of plasma membrane • Membrane ass. Disease response – 1. release of signal transduction molecules systematically 2. Release, accumulation of O radicals, lipoxygenases 3. Activation of phenol oxidases, oxidation of phenolics • O2-, H2O2, .OH released by multi subunit NADPH oxidase enzyme complex of plasma membrane • Sec or mins • Hydroperoxidation of membrane phospholipids, forming lipid hydroperoxides (toxic) • Involved in HR induced response • Oxidises phenols to more toxcs quinones • Lipoxygenases oxidizes membranes as well • Lipoxygenase generated hydroperoxides fom unsaturated fatty acids- lin, len →converted to bio active molecules- jasmonic acid role in wound and stress response Antimicrobials • Pathogenesis related proteins (PR)- toxic to invading fungi • Trace amounts normally, but high after pathogen attack (stress induced trancscription) • Extremely acidic or basic – hence soluble, reactive • PR1, chitinases, β 1,3-glucanases,proteinases, peroxidases, cystein rich proteins Phytoalexins • Antimicrobials produced by phytopathogens/ chemical/ mechanical injury • inhibit fungi, also toxic to bacteria, nematodes • Chemical structure- quite similar • Eg;- isoflavonoids in legumes • Accumulates around healthy cells around wounded cells • Phytoalexin elicitors- glucans, chitosan, glycoproteins (constituents of fungal cell wall) OTHER MECHANISMS • SIMPLE PHENOLICS- chlorogenic acid, caffeic acid • TOXIC PHENOLICS FROM NON-TOXIC PHENOL GLYCOSIDES (sugar+ phenolic)- microbial glycosidases • DETOXIFICATION OF PATHOGEN TOXINSEg:-fungal HC toxin (Cochliobolus carbonum), Pyricularin (Magnoporthe grisea)