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Plant stress responses
 

Plant stress responses

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    Plant stress responses Plant stress responses Presentation Transcript

    • 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
      • Abiotic (phy/che environment)
      • Biotic (organisms)
      • Abiotic- water logging, drought, high or low temperatures, excessive soil salinity, inadequate mineral nutrients, too much or too little light, ozone
      • STRESS FACTOR (stressor) – stress stimulus
      • STRESS RESPONSE (state of stress)- response to stimulus + ensuing state of adaptation
      • Avoidance of stress (protective)
      • Tolerance
      • Dynamics of stress- destabilizing, destructive component ( distress ) + counter mechanisms to promote restabilization and resistance ( eustress )
    • RESISTANCE
      • Depends on
      • Species
      • Genotype
      • Devt. Age of plant
      • Tissue identity
      • Duration, severity, rate of stress
      • 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 abiotic stress
      • Induced by many environmental conditions:
      • No rainfall- drought
      • High salt conc.
      • Low temp.
      • Transient loss of turgor at midday
      • Rate of onset, duration, acclimatization- influence the water stress response
    • Response to water deficit
      • ABA phytohormone
      • Induce expression of drought- inducible genes
      • Products- 2 groups
      • GROUP 1
      • Protective proteins (AFP, osmotins, chaperons, mRNA binding proteins)
      • Water channel proteins, membrane transporters
      • Osmoregulator synthesizing enzymes
      • Detoxifying enzymes (peroxidases, catalases)
    •  
      • B) GROUP 2
      • Transcription factors (DREB, MYC)
      • Protein kinases (MAP kinases, CDP kinases)
      • Proteinases (phospholipase)
      • 4 independent pathways
      • 2 - ABA-dependent
      • 2 - ABA- independent
      • Cis acting elements- in promoter of all stress inducible genes-
      • ABA-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 acids- degree of tolerance, particularly in plastids
      • Non- acclimatized plants- killed or injured at -10 0 C or below.
      • Freeze acclimatized trees- survive between -40 to -50 0 C
      • Injury- by severe dehydration during freeze-thaw cycles
      • Temp below 0 0 C , 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
      • Oxidation-
      • choline (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 Ca 2+ conc. In cytoplasm- Key component of Na+ signalling
      • SOS3 – Ca 2+ 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 mechanisms-
      • Reducing Na+ entry to cells
      • Na+ efflux from cell (K+-Na+)
      • 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) proteins- activated
    • 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 5 o 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 responses-stem 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- activated- products that inhibit pathogen
      • Signals to adjacent cells, usually systematically
      • Intracellular signal transducers- protein kinases, Ca 2+ ,phosphorylases, phospholipases, ATPases, H 2 O 2 ,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, enzymes-permeability changes of plasma membrane
      • Membrane ass. Disease response –
      • release of signal transduction molecules systematically
      • Release, accumulation of O radicals, lipoxygenases
      • Activation of phenol oxidases, oxidation of phenolics
    •  
      • O 2- , H 2 O 2 , .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 TOXINS-
      • Eg:-fungal HC toxin (Cochliobolus carbonum ),
      • Pyricularin (Magnoporthe grisea)