Plant stress

WATER DEFICIT
Euxerophyte/Drought tolerant- exhibit dehydration tolerance, rather than avoidance
Stenoxerophyte/drought excapers- complete their life cycle in wet season
Xerophytic nature exhibited by mainly 2 modes-
1. Dessication postponement- ability to maintain tissue hydration
I. Water savers- use water conservely
II. Water spenders-aggressively consume water
2. Dessication tolerance- ability to function when dehydrated.

Morphological adaptation:
1. Water content Turgor pressure [solute]plasma membrane thickenedcell shrunk Leaf area
Cell expansion GR=m(P-Y)
GR=growth rate; P=turgor pressure; Y= yield threshold; m=wall extensibility
2. Leaf absicission reults largely from enhanced synthesis of ethylene
3. Root extension, root resistance (resistance to lose water). Root to shoot biomass ration is governed by
water uptake and photosynthesis. A shoot will grow until their demand for photosynthesis from root equals
the supply.
4. Presence of sunken stomata (deeply seeded).
5. Stem becomes phylloclade.
6. heavy pubescence on leafwax deposition
7. transpirationphylotaxical changes paraheliotropic (leafs away from sun)

Physiological acclimatization:
1. Osmotic adjustment- plants can only absorb water if its water potential is more negative than its
surrounding soil. w= s+ p; w=water potential; s=solute potential; p=turgor potential.
s can be adjusted by in specific solutes-amino acid like proline, quarternary amines like glycine betaine,
sugar alcohol like mannitol, sorbitol, ions like K+ (restricted to vacuole; these may hamper enzyme action)
2. CAM photosynthesis- stomata open at night only, transpiration. ability to gain dry matter, this involves
PEPcase, pyruvate orthophosphate dikinase, NADP malic enzyme.
3. dormant seed strategy desert ephemerals escape drought by existing only as dormant seed during dry
season.
4. Xylem cavitation- embolism of water in xylem causing cohesive force and capillary action, so limit
transpiration.
5. root resistance- root move away from dry soil and hypodermis become more extensively covered by
suberin.
6. Protochlorophyll production

Regulation of gene expression:

Expression of osmotic stress handling genes are triggered
1 - Pyrroline-5-carboxy synthase-proline biosynthesis
 Plant stress

betaine aldehyde dehydrogenase- glycine betaine biosynthesis

myo-inositol-6-O-methyl transferase sugar alcohol (pinnitol)
gly-3-p-dehydrogenase- carbon flow; organic solute
ATPases, aquaporins- membrane transport
protease, ubiquitin, HSP- cleavage of denatured protein or renaturing them
SAM biosynthase- lignin biosynthesis

Stomatal physiology:
When guard cell lose their turgor due to water loss stomatal closure occur known as hydropassive
closure
When whole plant dehydrated reduction of solute content leads to lose turgor and stomata closes known as
hydroactive closure.

Abscisic acid:
ABA continuously synthesized in mesophyll but redistribute after water deficit. Since ABA is a weak acid the
anion form of ABA accumulates in alkaline stroma where it conjugates with H+ to form ABAH and cross
membrane to reach mesophyll
But in stress alkalinization reduced so ABA- form remained, thus cannot cross membrane, there by reach
guard cell by transpiration stream.
I. ABA [Ca2+ ] in cytoplasm that leads to stomatal closure. (mutants lacking functional ABA exhibit
permanent wilting- wilty mutants)
II. ABA shoot growth & root growth
III. Low [ABA] conductance of water through root
IV. Promote leaf senescence and ethylene production.

WATER Logging
Morphological
1. Aerenchyma formation: External O2 shortagehypoxic cortexethylenecortical cell signal
transduction activation of suicide gene cell death Aerenchyma formation.
2. reorientation of leaves and stem: Anaerobsis in root ACC synthase ACC production from SAM
ethylene intermodal shoot elongation
3. root replacement and reorientation
4. Fast shoot elongation expansin expression
Biochemical
1. HIP (hypoxically induced protein) by MyB, G-box factor, 14-3-3 that binds to anaerobic response element.
metabolic theory= Alcohol Dehydrogenase ethanol toxicity shift of glycolytic intermediates to
malate , lactate etc tolerance Lactate LDH acidification of cytoplasm [O2] Water logging =
pH stat hypothesis
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SALINITY stress

Glycophytes- sensitive to [salt]; Halophytes- able to grow in [salt]

Accumulators- Osmotic potential continue to become ve. Water enter through endodermis, not bulk flow.
Succulents- shoot or leaves swell by absorbing water to dilute high salt that enter with wate.
Regulators-[salt] does in these plants, they regulate salt balance through different ways-

1. Salt exclusion
I. Preferential loading of K+ rather than Na+ by stellar cell in xylem
II. Removal of salt from upper part of xylem in petiole, stem or leaf sheaths
2. Ion homeostasis-
I. H+ pumps p type ATPase, provide H+ gradient to compartmentalize cytotoxic ion, preferentially
control Na+ influx across endodermis.
II. Regulation of Na+ influx- Na+ influx is directly inhibited by Ca2+, efflux is mediated by gene product
of SOS1.
3. Compartmentalization- compartmentalization of Na+ by Na+-H+ antiporter (eg. AtNHX1 of Arabidopsis)
4. SOS signaling
I. Hyperosmotic component of high salinity influx of Ca2+ throughCch1p and Mid1p [Ca2+]cyt
PP2B phosphatase (Calcineurin) expression of ENA1(p type ATPase) Na+ efflux.
II. SOS3 (salt overly sensitive) encodes a Ca2+ binding domain interaction with SOS2 upon Ca2+
binding SOS2 get activated activate Na+-H+ antiporter SOS1.
5. Exudation by salt gland- Secrete NaCl in exchange absorb water hydroscopically (Nolana mollis)
6. Osmotic Adjustment
Compatible solutes in cytoplasm functions in osmoprotection. K+ is the only ion others are organic molecules.
I. Simple sugars- Fructose and Glucose
II. Sugar alcohols- glycerol, methylated inositols, pinnitol, mannitols, sorbitols
III. Complex sugars- Trehalose, raffinose, fructans
IV. Amino acid derivative- Proline, glycine betaine, alanine betaine, proline betaine
V. Tertiary amine- 1,4,5,6-tetrahydro-2-M-carboxyl pyrimidine
VI. Sulphonamide derivative- choline-o-sulfate, dimethyl sulphonium propionate

LOW TEMPERATURE stress

Chilling Injury- A fall of temp. to 10-12C causes a slowing of growth, discoloration, lesions on leaves,
foliage looks sloggy, this is chilling injury.
Freezing injury- this type of injury occurs below the freezing point of water. Induction of ice formation and
thereby dehydration of chloroplast.

Protection mechanism:
1. Membrane properties change- desaturase activity, unsaturation of fatty acid, chain length of fatty
acid,
 Plant stress

2. Limitation of Ice nucleation-

I. Antifreeze proteins- It confer the cell sap the property of thermal hysteresis ( transition of liquid to
solid promoted at lower temp, than transition from solid to liquid). It works by trypsin like activity,
chewing ice crystals to break them.
II. Sugars- sugars like sucrose also lowers ice nucleation
3. Deep super cooling cell protoplast suppress ice nucleation and cell wall act as barriers for dehydration,
in such condition water inside xylem in most deciduous plants do not freeze unless the temp drops as low as
-40C.
4. Pathogenesis related proteins- when temp falls to -3C to -5C, some bacteria (eg. Pseudomonas
syringae) induce ice formation. Some antifreeze proteins of endochitinase or endoglucanase family act
against these pathogens.
5. Gene expression- CBF/DREB1 binds to CRE/DRE and induce many cold stress protein expression
6. ABA appears to promote freezing tolerance
7. Needle shaped leaves, short height (capillary action 34 feet)