Download BIOTIC STRESSES

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
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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
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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
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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
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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)