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Plant stress responses

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Plant stress responses

  1. 1. PLANT STRESS RESPONSE
  2. 2. STRESS <ul><li>Manifold unfavourable, but not necessarily immediately lethal conditions, occurring either permanently or sporadically in a locality </li></ul><ul><li>Significant deviation from optimal conditions for life </li></ul><ul><li>Elicit responses and changes at all functional levels of the organism </li></ul><ul><li>May be first reversible, but may become permanent </li></ul>
  3. 3. STRESS <ul><li>Conditions that adversely affect growth, development, productivity </li></ul><ul><li>Abiotic (phy/che environment) </li></ul><ul><li>Biotic (organisms) </li></ul><ul><li>Abiotic- water logging, drought, high or low temperatures, excessive soil salinity, inadequate mineral nutrients, too much or too little light, ozone </li></ul>
  4. 4. <ul><li>STRESS FACTOR (stressor) – stress stimulus </li></ul><ul><li>STRESS RESPONSE (state of stress)- response to stimulus + ensuing state of adaptation </li></ul><ul><li>Avoidance of stress (protective) </li></ul><ul><li>Tolerance </li></ul><ul><li>Dynamics of stress- destabilizing, destructive component ( distress ) + counter mechanisms to promote restabilization and resistance ( eustress ) </li></ul>
  5. 5. RESISTANCE <ul><li>Depends on </li></ul><ul><li>Species </li></ul><ul><li>Genotype </li></ul><ul><li>Devt. Age of plant </li></ul><ul><li>Tissue identity </li></ul><ul><li>Duration, severity, rate of stress </li></ul>
  6. 6. <ul><li>Alarm phase – stress reaction </li></ul><ul><li>Restitution- repair </li></ul><ul><li>Hardening </li></ul><ul><li>Adjustment </li></ul><ul><li>Adaptation- normalization </li></ul><ul><li>(Exhaustion)- irreversible damage </li></ul><ul><li>End phase </li></ul>
  7. 7. STRESS RESPONSE <ul><li>Race b/w effort to adapt and potentially lethal processes in protoplasm </li></ul><ul><li>Triggered by stress or stress- induced injury (membrane integrity loss) </li></ul><ul><li>Some- enable plant to acclimatize to stress </li></ul>
  8. 8. <ul><li>Altered gene expression- changes in development, metabolism </li></ul><ul><li>Initiated when plant recognizes stress at cellular level- proteins that sense abiotic stress </li></ul><ul><li>Transmit information within individual cells and through out the plant </li></ul><ul><li>increase in specific mRNA, enhanced translation, stabilization of proteins, alteration of protein activity </li></ul>
  9. 9. WATER DEFICIT <ul><li>Major abiotic stress </li></ul><ul><li>Induced by many environmental conditions: </li></ul><ul><li>No rainfall- drought </li></ul><ul><li>High salt conc. </li></ul><ul><li>Low temp. </li></ul><ul><li>Transient loss of turgor at midday </li></ul><ul><li>Rate of onset, duration, acclimatization- influence the water stress response </li></ul>
  10. 10. Response to water deficit <ul><li>ABA phytohormone </li></ul><ul><li>Induce expression of drought- inducible genes </li></ul><ul><li>Products- 2 groups </li></ul><ul><li>GROUP 1 </li></ul><ul><li>Protective proteins (AFP, osmotins, chaperons, mRNA binding proteins) </li></ul><ul><li>Water channel proteins, membrane transporters </li></ul><ul><li>Osmoregulator synthesizing enzymes </li></ul><ul><li>Detoxifying enzymes (peroxidases, catalases) </li></ul>
  11. 12. <ul><li>B) GROUP 2 </li></ul><ul><li>Transcription factors (DREB, MYC) </li></ul><ul><li>Protein kinases (MAP kinases, CDP kinases) </li></ul><ul><li>Proteinases (phospholipase) </li></ul>
  12. 13. <ul><li>4 independent pathways </li></ul><ul><li>2 - ABA-dependent </li></ul><ul><li>2 - ABA- independent </li></ul><ul><li>Cis acting elements- in promoter of all stress inducible genes- </li></ul><ul><li>ABA-responsive element (ABRE) </li></ul><ul><li>dehydration responsive element (DREB) </li></ul>
  13. 14. COLD- STRESS <ul><li>Plants produce a no. of proteins in response to cold and freezing temp. </li></ul><ul><li>54 cold inducible genes </li></ul><ul><li>10% of drought induced genes- also induced by cold </li></ul><ul><li>Genes- contain a cis element repeat (CRT)- 5 bp seq. </li></ul><ul><li>Transcription factor- C repeat binding factor (CBF)- Main controlling switch in monocots, dicots </li></ul>
  14. 15. Cold stress reactions <ul><li>Injury to cell membrane – chilling, freezing </li></ul><ul><li>Ratio of saturated to unsaturated fatty acids- degree of tolerance, particularly in plastids </li></ul><ul><li>Non- acclimatized plants- killed or injured at -10 0 C or below. </li></ul><ul><li>Freeze acclimatized trees- survive between -40 to -50 0 C </li></ul><ul><li>Injury- by severe dehydration during freeze-thaw cycles </li></ul>
  15. 16. <ul><li>Temp below 0 0 C , cellular water freeze. </li></ul><ul><li>Cell shrinkage </li></ul><ul><li>Expansion induced lysis </li></ul>
  16. 17. <ul><li>SURVIVAL STRATEGIES: </li></ul><ul><li>anti freeze proteins (AFP) </li></ul><ul><li>Declines rate of ice crystal growth </li></ul><ul><li>Lowers the efficiency of ice nucleation sites </li></ul><ul><li>Lowers temp. at which ice forms </li></ul><ul><li>Osmoprotectants </li></ul><ul><li>osmolytes- quarternary amines, amino acids, sugar alcohols </li></ul><ul><li>Balances the osmotic potential of externally increased osmotic pressure </li></ul>
  17. 18. <ul><li>Glycine betaine </li></ul><ul><li>Quaternary amine, soluble </li></ul><ul><li>CH3 gps- interact with hydrophobic and hydrophilic molecules </li></ul><ul><li>Oxidation- </li></ul><ul><li>choline (choline monooxygenase) > betaine aldehyde </li></ul><ul><li>Betaine aldehyde (betaine aldehyde dehydrogenase) > glycine betaine </li></ul>
  18. 19. <ul><li>Proline </li></ul>
  19. 20. <ul><li>Sugar alcohols –mannitol </li></ul><ul><li>Trehalose- non reducing disaccharide </li></ul><ul><li>Increased water retention and desiccation tolerance </li></ul>
  20. 21. SALT STRESS <ul><li>Flow of water is reversed- imbalance </li></ul><ul><li>Accumulation of excess Na+, Cl- in cytosol </li></ul><ul><li>Stress tolerant plants- maintains internal osmotic pressure </li></ul>
  21. 22. Sensing salt stress <ul><li>Ion specific signals of salt stress </li></ul><ul><li>High Na+- increases Ca 2+ conc. In cytoplasm- Key component of Na+ signalling </li></ul><ul><li>SOS3 – Ca 2+ binding protein </li></ul><ul><li>Activates protein kinase (SOS2) </li></ul><ul><li>Phosphorylates (activates) plasma membrane H+-Na+ antiporter (SOS1) </li></ul><ul><li>SOS1 mRNA- stabilized, accumulates </li></ul><ul><li>- </li></ul>
  22. 23. <ul><li>Plant maintains high K+, low Na+ in cytosol </li></ul><ul><li>3 tolerance mechanisms- </li></ul><ul><li>Reducing Na+ entry to cells </li></ul><ul><li>Na+ efflux from cell (K+-Na+) </li></ul><ul><li>Active transport to vacuole (vacuolar H+-Na+ ATPase) </li></ul>
  23. 25. Na+ sequestration <ul><li>In vacuoles </li></ul><ul><li>By NHX1, NHX2 proteins of tonoplast membrane </li></ul><ul><li>Decreases cytoplasmic Na+ </li></ul>
  24. 26. Salt stress induced proteins <ul><li>Transcription of genes oncoding late embryogenesis abundant (LEA) proteins- activated </li></ul>
  25. 27. Antioxidant production <ul><li>Abiotic stress – drought, salt, chill- increases reactive O intermediates (ROI) in plants </li></ul><ul><li>ROI- stress signal- due to altered metabolic functions of chloroplast, mitochondria </li></ul><ul><li>ROI SCAVENGING </li></ul><ul><li>Antioxidant system contains a battery of enzymes that scavenge ROI- SOD, peroxidases, catalases, glutathione reductases </li></ul>
  26. 28. HEAT STRESS <ul><li>Decrease in synthesize of normal proteins </li></ul><ul><li>Transcription and translation of HSPs </li></ul><ul><li>When 5 o C rise in optimum temp. </li></ul><ul><li>Conserved proteins </li></ul><ul><li>Act as chaperons, refolding </li></ul><ul><li>classes- based on mw </li></ul><ul><li>Hsp 100, Hsp 90, Hsp 70, Hsp60 </li></ul>
  27. 30. FLOODING <ul><li>-Decreases O2 availability of plant roots </li></ul><ul><li>-ATP production is lowered </li></ul><ul><li>-SURVIVAL STRATEGIES: production of enzymes for sucrose, starch degradation, glycolysis, ethanol fermentation </li></ul><ul><li>-ethylene- long term acclimatization responses-stem elongation </li></ul>
  28. 32. BIOTIC STRESSES
  29. 34. INDUCED STRUCTURAL AND BIOCHEMICAL DEFENCES <ul><li>Plants receive signal molecules as soon as pathogen contact </li></ul><ul><li>Elicitors of recognition </li></ul><ul><li>Host receptors – on plasma membrane or cytoplasm </li></ul><ul><li>Bichemical reactions, structural changes – to fend off pathogen, toxins </li></ul>
  30. 36. Signal transduction <ul><li>Transmission of alarm signal to host defense providers </li></ul><ul><li>To host proteins, nucleur genes- activated- products that inhibit pathogen </li></ul><ul><li>Signals to adjacent cells, usually systematically </li></ul><ul><li>Intracellular signal transducers- protein kinases, Ca 2+ ,phosphorylases, phospholipases, ATPases, H 2 O 2 ,ethylene. </li></ul>
  31. 38. <ul><li>Systemic signal transduction, aquired resistance- by salicylic acid, oligogalacturonides from plant cell walls, jasmonic acid, systemin, fatty acids, ethylene </li></ul>
  32. 39. Induced structural defenses <ul><li>After pathogen has penetrated preformed defense structures- plant respond by one or more structures to prevent further pathogen invasion </li></ul><ul><li>Defense structures : </li></ul><ul><li>1) cytoplasmic defense reaction </li></ul><ul><li>2) cell wall defense structures </li></ul><ul><li>3) histological dfense structures </li></ul><ul><li>4) necrotic/ hypersensitive defense reaction </li></ul>
  33. 40. Cytoplasmic defense reaction <ul><li>In response to weakly pathogenic and mycorrhizal fungi </li></ul><ul><li>Induce chronic diseases / nearly symbiotic conditions </li></ul><ul><li>Cytoplasm surrounds hyphal clump </li></ul><ul><li>Cytoplasm and nucleus enlarge </li></ul><ul><li>Dense granular cytoplasm </li></ul><ul><li>Mycelium disintegrates, invasion stops. </li></ul>
  34. 41. Cell wall defense structures <ul><li>Morphological changes of cell wall </li></ul><ul><li>Limited effectiveness </li></ul><ul><li>a) parenchymatous cells’ walls swell, produces amorphous, fibrillar material that surrounds, traps bacteria </li></ul><ul><li>b) cell wall thickens by a cellulosic material infused with phenolics </li></ul><ul><li>c) callose papillae laid of inner surface of cell wall (2-3 mins ) (fungi) </li></ul><ul><li>formation of lignituber around fungal hyphae </li></ul>
  35. 42. Histological defense structures <ul><li>Formation of cork layers- fungi, bacteria, virus, nematodes </li></ul><ul><li>inhibits invasion beyond initial lesion </li></ul><ul><li>prevents flow of nutrients </li></ul><ul><li>Abscission layers- fungi, bacteria, virus </li></ul><ul><li>gap b/w 2 circular cell layers surrounding infection site </li></ul><ul><li>Tyloses - over growth of protoplasts of adjacent parenchymatous cells- protrude into xylem vessels through piths </li></ul><ul><li>Gums - around lesions </li></ul><ul><li>intracellular spaces, within surr. cells. </li></ul>
  36. 43. ABSCISSION LAYER
  37. 44. TYLOSE FORMATION
  38. 45. Necrotic defense reaction <ul><li>Hypersensitive response </li></ul><ul><li>Brown resin-like granules in cytoplasm </li></ul><ul><li>Browning continues, cell dies </li></ul><ul><li>Invading hypha- degenerates </li></ul><ul><li>Bacterial infections- destruction of cell membranes, desiccation, necrosis of tissue </li></ul><ul><li>Obligate parasites- fungi, bacteria, nematode, viruses </li></ul>
  39. 46. INDUCED BIOCHEMICAL DEFENSES <ul><li>HYPERSENSITIVE RESPONSE(HR) </li></ul><ul><li>Initiated by elicitor recognition </li></ul><ul><li>Rapid burst of oxidative reactions </li></ul><ul><li>↑ sed ion movement (H+, K+) </li></ul><ul><li>Loss of cellular compartmentalization </li></ul><ul><li>Crosslinking of phenolics with cell wall </li></ul><ul><li>Production of antimicrobials </li></ul>
  40. 47. HR
  41. 49. <ul><li>due to plant R (resistance) gene </li></ul><ul><li>Pathogen produced elicitor- from its Avirulence gene </li></ul><ul><li>Eg:- arv D gene of P. syringae- enzyme involved in synthesis of syringolides (hypersensitive response in soya bean) </li></ul><ul><li>Eg:- protein of tobacco R gene- protect against leaf spotting bacterium – in cytoplasm </li></ul><ul><li>Eg:- protein of Cf9 R gene of tomato- against race 9 of leaf mould fungus- outside plasma membrane </li></ul>
  42. 50. ACTIVE O RADICALS, LIPOXYGENASES, CELL MEMBRANE DISRUPTION <ul><li>Pathogen attack, exposure to toxins, enzymes-permeability changes of plasma membrane </li></ul><ul><li>Membrane ass. Disease response – </li></ul><ul><li>release of signal transduction molecules systematically </li></ul><ul><li>Release, accumulation of O radicals, lipoxygenases </li></ul><ul><li>Activation of phenol oxidases, oxidation of phenolics </li></ul>
  43. 52. <ul><li>O 2- , H 2 O 2 , .OH released by multi subunit NADPH oxidase enzyme complex of plasma membrane </li></ul><ul><li>Sec or mins </li></ul><ul><li>Hydroperoxidation of membrane phospholipids, forming lipid hydroperoxides (toxic) </li></ul><ul><li>Involved in HR induced response </li></ul><ul><li>Oxidises phenols to more toxcs quinones </li></ul><ul><li>Lipoxygenases oxidizes membranes as well </li></ul>
  44. 53. <ul><li>Lipoxygenase generated hydroperoxides fom unsaturated fatty acids- lin, len </li></ul><ul><li>-> converted to bio active molecules- jasmonic acid </li></ul><ul><li>role in wound and stress response </li></ul>
  45. 56. Antimicrobials <ul><li>Pathogenesis related proteins (PR)- toxic to invading fungi </li></ul><ul><li>Trace amounts normally, but high after pathogen attack (stress induced trancscription) </li></ul><ul><li>Extremely acidic or basic – hence soluble, reactive </li></ul><ul><li>PR1, chitinases, β 1,3-glucanases,proteinases, peroxidases, cystein rich proteins </li></ul>
  46. 57. Phytoalexins <ul><li>Antimicrobials produced by phytopathogens / chemical/ mechanical injury </li></ul><ul><li>inhibit fungi, also toxic to bacteria, nematodes </li></ul><ul><li>Chemical structure- quite similar </li></ul><ul><li>Eg;- isoflavonoids in legumes </li></ul><ul><li>Accumulates around healthy cells around wounded cells </li></ul><ul><li>Phytoalexin elicitors- glucans, chitosan, glycoproteins (constituents of fungal cell wall) </li></ul>
  47. 59. OTHER MECHANISMS <ul><li>SIMPLE PHENOLICS- chlorogenic acid, caffeic acid </li></ul><ul><li>TOXIC PHENOLICS FROM NON-TOXIC PHENOL GLYCOSIDES (sugar+ phenolic)- microbial glycosidases </li></ul><ul><li>DETOXIFICATION OF PATHOGEN TOXINS- </li></ul><ul><li>Eg:-fungal HC toxin (Cochliobolus carbonum ), </li></ul><ul><li>Pyricularin (Magnoporthe grisea) </li></ul>

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