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

RESISTANCE Depends on Species Genotype 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 a biotic 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 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 -100 C or below. Freeze acclimatized trees- survive between -40 to -500C Injury- by severe dehydration during freeze-thaw 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 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 Ca2+ conc. In cytoplasm- Key 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 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 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 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, 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, 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

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 TOXINS- Eg:-fungal HC toxin (Cochliobolus carbonum), Pyricularin (Magnoporthe grisea)