Abscisic Acid (ABA)
Abscisic Acid (ABA):-
> It is found in older leaves, apical buds and seeds.
> Both GA and ABA hormones work opposite to each other.
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> ABA inhibits the biosynthesis of the hormone GA.
1. Chemical nature of Abscisic Acid:- This phytohormone is a 15-carbon sesquiterpene and its synonyms are dormin and abscisin-II.
3. Physiological effects of Abscisic Acid:-
i. Seed and bud dormancy:- Its main function is to maintain seed dormancy. Abscisic acid induces dormancy of buds towards the approach of winter. Abscisic acid accumulates in many seeds during maturation and apparently contributes to seed dormancy.
ii. Senescence:- ABA acts as a general inducer of senescence (Thimann). The onset of senescence is correlated with stomatal closure. The ABA content of aging leaves increases markedly as senescence is initiated.
iii. Abscission:- It is the process of shedding old or unwanted organs such as leaves, flower, floral organs, and fruits. ABA promotes abscission through ethylene.
iv. Flowering:- In long-day plants, the effect of gibberellins on flowering is counteracted by ABA, which accumulated in the leaves during the short winter days. This ABA acts as inhibitor of flowering in long-day plants. On the other hand ABA induces flowering in short-day plants.
v. Starch hydrolysis:- The GA-induced synthesis of a-amylase and other hydrolytic enzymes in barley aleurone cells is inhibited by abscisic acid. This inhibition can be reversed by increasing the amount of GA supplied.
vi. Geotropism:- ABA controls geotropic responses of roots. It stimulates positive geotropism in roots.
vii. Stress response:- It also close the stomata of the leaves in dry conditions. Hence it is also called stress hormone.
4. Mode of Action of Abscisic Acid:-
a. Regulation of Gene Expression and Enzyme Synthesis:-
> ABA has inhibitory effects on protein synthesis. The effect of ABA on protein synthesis appears to be selective since it has been shown to affect directly the synthesis of those proteins whose synthesis is under hormonal control.
> The best example of such translational control is the inhibition by ABA of the GA-promoted synthesis of α-amylase and other hydrolases like protease and ribonuclease in barley aleurone layers.
> Ho and Varner suggested that the inhibition of a-amylase synthesis by ABA is due to an effect on translation, since they found that ABA still inhibited the formation of α-amylase at 12 h, a time when RNA synthesis inhibitor cordycepin had no longer any effect.
> They have postulated that ABA might de-repress a regulator gene or interact with a regulator RNA protein species to inhibit the translation of α-amylase mRNA.
> ABA has regulatory effects at the levels of both transcription and translation. The expression of numerous genes is stimulated by ABA under various stress conditions. Such conditions include heat shock, low temperature and salinity stress as well as the period of seed maturation.
> It is well known that gene activation is mediated by DNA-binding proteins, which acts as transcription factors. ABA has been shown to stimulate the transcription of the genes, which encode these binding proteins.
> Distinct DNA segments have been identified that are involved in stimulation of transcription by ABA, thought to be ABA-response elements (ABAREs). Contrary to the stimulation of gene expression, ABA is also involved in repression of gene transcription.
> The common example is ABA-induced repression of barley a-amylase gene which is expressed by GA. In this case, a few DNA elements which mediate ABA-induced gene repression are quite similar to the gibberellin response elements (GAREs).
b. Stomatal Complexes and ABA:-
> Turgor changes within the guard cells regulate stomatal aperture. Such turgor changes are caused by movement of K+, H+, Cl– ions and the synthesis, metabolism and movement of organic anions, particularly malate. The role of ABA in these movements and synthesis is still a matter of conjecture.
> One important factor in regulating guard-cell turgor is thought to be the operation of an active H+/K+ exchange process. ABA inhibits K+ uptake into the guard cells and also proton release. The fungal toxin fusicoccin (FC) overcomes the effect of ABA on the stomata by stimulating H+/K+ exchange. ABA may also affect the distribution of malate.
> During stomatal closure in dark, malate leaks from the epidermal strips of Commelina communis, Vicia faba floating on water. Addition of ABA increases both the rate of closure and the rate of malate leakage.
> Malate serves as a source of protons for H+/K+ exchange process during opening and malate leakage from guard cells during closure is required to reduce turgor. ABA would inhibit H+/K+ exchange and promote specific leakage of malate, thus inhibiting opening and promoting closure.
c. Membrane Depolarization by Increasing Ca2+ and pH of Cytosol:-
> Although stomatal closure is mediated by a reduction in guard cell turgor pressure caused by massive outward movement of K+ and anions (CI– and malate) from the cell, ABA also induces a net influx of positive charge.
> ABA has been shown to induce an increase in cytosolic Ca2+ concentration by activation of calcium channels leading to membrane depolarization. Cytosolic calcium concentration is further increased by ABA by causing release of calcium from an internal store like vacuole, and this increase is sufficient to cause stomatal closing.
> In addition to increasing cytosolic Ca2+, ABA causes alkalization of the cytosol. The increase in cytosolic pH triggers the voltage-gated K+ efflux channels to open resulting in K+ loss and stomatal closure.
> The inhibition of plasma membrane H+-ATPase has also been held responsible for membrane depolarization. ABA inhibits the plasma membrane proton pump and favours depolarization in an indirect manner. It is presumed that the increase in Ca2+ concentration and pH of the cytosol in the presence of ABA results in the inhibition of H+ -ATPase.
> ABA not only causes stomatal closure by activating outward ion channels but also prevents stomatal opening. Under normal conditions, the inward K+ channels are open when the membrane is polarized by the proton pump and K+ ions get inside through H+/K+ exchange causing stomatal opening. In this case, ABA inhibits inward K+ channels through an increase in Ca2+ and pH, thus preventing stomatal opening.
