ABA functions in many plant developmental processes, including seed and bud dormancy, the control of organ size and stomatal closure.

[6] 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.

[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.

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.

A close linear correlation was found between the ABA content of the leaves and their conductance (stomatal resistance) on a leaf area basis.

[citation needed] Abscisic acid (ABA) is an isoprenoid plant hormone, which is synthesized in the plastidal 2-C-methyl-D-erythritol-4-phosphate (MEP) pathway; unlike the structurally related sesquiterpenes, which are formed from the mevalonic acid-derived precursor farnesyl diphosphate (FDP), the C15 backbone of ABA is formed after cleavage of C40 carotenoids in MEP.

[20] In soil bacteria, an alternative catabolic pathway leading to dehydrovomifoliol via the enzyme vomifoliol dehydrogenase has been reported.

[citation needed] Like plants, some fungal species (for example Cercospora rosicola, Botrytis cinerea[28] and Magnaporthe oryzae) have an endogenous biosynthesis pathway for ABA.

ABA elicits potent anti-inflammatory and anti-diabetic effects in mouse models of diabetes/obesity, inflammatory bowel disease, atherosclerosis and influenza infection.

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.