In the 1940s, Torsten Hemberg, while working at the University of Stockholm, found evidence that a positive correlation exists between the rest period and the occurrence of an acidic ether soluble growth inhibitor in
potato tubers.[7][8]
In 1963, abscisic acid was first identified and characterized as a plant hormone by Frederick T. Addicott and Larry A. Davis. They were studying compounds that cause
abscission (shedding) of
cotton fruits (bolls). Two compounds were isolated and called
abscisin I and abscisin II. Abscisin II is presently called abscisic acid (ABA).[5]
In plants
Function
ABA was originally believed to be involved in
abscission, which is how it received its name. This is now known to be the case only in a small number of plants. ABA-mediated signaling also plays an important part in plant responses to environmental stress and plant pathogens.[9][10] The plant genes for ABA biosynthesis and sequence of the pathway have been elucidated.[11][12] ABA is also produced by some plant pathogenic fungi via a biosynthetic route different from ABA biosynthesis in plants.[13]
In preparation for winter, ABA is produced in
terminal buds.[14] This slows plant growth and directs leaf
primordia to develop scales to protect the dormant buds during the cold season. ABA also inhibits the division of cells in the
vascular cambium, adjusting to cold conditions in the winter by suspending primary and secondary growth.
Abscisic acid is also produced in the
roots in response to decreased soil
water potential (which is associated with dry soil) and other situations in which the plant may be under stress. ABA then translocates to the leaves, where it rapidly alters the osmotic potential of stomatal
guard cells, causing them to shrink and
stomata to close. The ABA-induced stomatal closure reduces
transpiration (evaporation of water out of the stomata), thus preventing further water loss from the leaves in times of low water availability. A close linear correlation was found between the ABA content of the leaves and their conductance (stomatal resistance) on a leaf area basis.[15]
Several ABA-
mutantArabidopsis thaliana plants have been identified and are available from the
Nottingham Arabidopsis Stock Centre - both those deficient in ABA production and those with altered sensitivity to its action. Plants that are hypersensitive or insensitive to ABA show phenotypes in
seed dormancy,
germination,
stomatal regulation, and some mutants show stunted growth and brown/yellow leaves. These mutants reflect the importance of ABA in seed germination and early embryo development.[citation needed]
Abamine has been designed, synthesized, developed and then patented as the first specific ABA biosynthesis inhibitor, which makes it possible to regulate endogenous levels of ABA.[17]
Locations and timing of ABA biosynthesis
Synthesized in nearly all plant tissues, e.g., roots, flowers, leaves and
stems
Stored in
mesophyll (
chlorenchyma) cells where it is conjugated to glucose via uridine diphosphate-glucosyltransferase resulting in the inactivated form, ABA-glucose-ester [18]
Activated and released from the chlorenchyma in response to
environmental stress, such as heat stress, water stress, salt stress[18]
Synthesized in green
fruits at the beginning of the winter period
Synthesized in maturing
seeds, establishing
dormancy
Mobile within the
leaf and can be rapidly translocated from the leaves to the roots (opposite of previous belief) in the
phloem
Accumulation in the roots modifies lateral root development, improving the stress response
ABA is synthesized in almost all cells that contain chloroplasts or
amyloplasts
Inactivation
ABA can be catabolized to
phaseic acid via
CYP707A (a group of
P450 enzymes) or inactivated by glucose conjugation (ABA-glucose ester) via the enzyme uridine diphosphate-glucosyltransferase (UDP-glucosyltransferase). Catabolism via the CYP707As is very important for ABA homeostasis, and mutants in those genes generally accumulate higher levels of ABA than lines overexpressing ABA biosynthetic genes.[20] In soil bacteria, an alternative catabolic pathway leading to dehydrovomifoliol via the enzyme
vomifoliol dehydrogenase has been reported.
In the absence of ABA, the
phosphatase ABI1-INSENSITIVE1 (ABI1) inhibits the action of SNF1-related protein
kinases (subfamily 2) (SnRK2s). ABA is perceived by the PYRABACTIN RESISTANCE 1 (
PYR1) and PYR1-like membrane proteins. On ABA binding, PYR1 binds to and inhibits ABI1. When SnRK2s are released from inhibition, they activate several
transcription factors from the ABA RESPONSIVE ELEMENT-BINDING FACTOR (ABF) family. ABFs then go on to cause changes in the
expression of a large number of
genes.[6] Around 10% of plant genes are thought to be regulated by ABA.[citation needed]
In fungi
Like plants, some fungal species (for example Cercospora rosicola, Botrytis cinerea[28] and Magnaporthe oryzae) have an endogenous biosynthesis pathway for ABA. In fungi, it seems to be the
MVA biosynthetic pathway that is predominant (rather than the
MEP pathway that is responsible for ABA biosynthesis in plants). One role of ABA produced by these pathogens seems to be to suppress the plant immune responses.[29]
In animals
ABA has also been found to be present in
metazoans, from
sponges up to
mammals including humans.[30] Currently, its biosynthesis and biological role in animals is poorly known. ABA has recently been shown to elicit potent anti-inflammatory and anti-diabetic effects in mouse models of diabetes/obesity, inflammatory bowel disease, atherosclerosis and influenza infection.[31] Many biological effects in animals have been studied using ABA as a
nutraceutical or
pharmacognostic drug, but ABA is also generated endogenously by some cells (like
macrophages) when stimulated. There are also conflicting conclusions from different studies, where some claim that ABA is essential for pro-inflammatory responses whereas other show anti-inflammatory effects. Like with many natural substances with medical properties, ABA has become popular also in
naturopathy. While ABA clearly has beneficial biological activities[citation needed] and many naturopathic remedies will contain high levels of ABA (such as
wheatgrass juice, fruits and vegetables), some of the health claims made may be exaggerated or overly optimistic. In mammalian cells ABA targets a protein known as
lanthionine synthetase C-like 2 (
LANCL2), triggering an alternative mechanism of activation of peroxisome proliferator-activated receptor gamma
(PPAR gamma).[32] LANCL2 is conserved in plants and was originally suggested to be an ABA receptor also in plants, which was later challenged.[33]
Measurement of ABA concentration
Several methods can help to quantify the concentration of abscisic acid in a variety of plant tissue. The quantitative methods used are based on
HPLC and
ELISA. Recently, 2 independent
FRET probes have been developed that can measure intracellular ABA concentrations in real time in vivo.[34][35]
^"Abscisic Acid - Compound Summary". PubChem Compound. USA: National Center for Biotechnology Information. 16 September 2004. Identification and Related Records. Retrieved 22 October 2011.
^Zhang, Jianhua; Schurr, U.; Davies, W. J. (1987). "Control of Stomatal Behaviour by Abscisic Acid which Apparently Originates in the Roots". Journal of Experimental Botany. 38 (7): 1174–1181.
doi:
10.1093/jxb/38.7.1174.
^Miernyk, J. A. (1979). "Abscisic Acid Inhibition of Kinetin Nucleotide Formation in Germinating Lettuce Seeds". Physiologia Plantarum. 45: 63–6.
doi:
10.1111/j.1399-3054.1979.tb01664.x.
^Chandler, P M; Robertson, M (1994). "Gene Expression Regulated by Abscisic Acid and its Relation to Stress Tolerance". Annual Review of Plant Physiology and Plant Molecular Biology. 45: 113–41.
doi:
10.1146/annurev.pp.45.060194.000553.