The dormancy observed in lateral buds and winter buds and embryos in seeds has been thought to be induced by some growth substance. In the 1960s two groups of plant physiologists reported isolating a compound. One group studying leaf abscission in cotton isolated abscisin, the other group studying dormant buds in sycamore isolated dormin. The two groups determined the chemical structures and they were identical. Plant physiologists determined that they should decide which name to use. The two groups met. The cotton group had money and was powerful in terms of personality; the sycamore group had less recognition and was less aggressive. They came out of their meeting with an agreement to call the chemical abscisic acid. To the rich go the spoils and fame.
However, in retrospect, the abscission story is really an ethylene-auxin situation. The role of abscisic acid in abscission was a pharmacological artifact...applied AbA often induces ethylene biosynthesis. So the rich and famous were wrong. The group that did the honest work on dormin were studying a true role for the chemical they isolated. The chemical, currently known as abscisic acid, should really be called dormin...hence my title for this lecture.
You will notice that most plant physiology textbooks cite the work for abscisic acid done by members of the the rich and famous but wrong. However, while the work of the other group is mentioned, the work and the names are not cited at all. My complaint about "in crowdism" in American plant physiology circles applies to this situation as well.
Here is the chemical structure of dormin and related molecules.
A careful look at this structure shows it to be isoprene-based. Its synthesis pathway is shown below. The isoprene units are assembled and along the way our old friend from blue-light responses, zeaxanthin, is an intermediate!
In the second part of the synthesis the xeaxanthin is cleaved to release the growth regulating substances including AbA-aldehyde. In the final part of the synthesis of dormin, the finishing touches are made to create the active hormone.
As you might notice above, there are mutants in many species that have a defective enzyme in the synthesis of abscisic acid. None of them are named for some failure of leavers to abscise because this name is false. Several of the mutants are labeled vp which stands for "viviparous." Below is an AbA synthesis mutant in corn. You can see that the embryos do not receive the dormin needed to achieve and maintain the dormancy of the embryo. So the embryo never goes dormant, the seeds do not desiccate properly, and the embryos sprout prematurely. This mutant is called viviparous for obvious reasons. This image puts a huge exclamation point on our understanding of the politics of plant physiology. This chemical should be called DORMIN !
As we have seen with other growth regulators, dormin can be conjugated to sugars, and can be oxidized to phaseic acid and dihydrophaseic acid. In either case these reactions are unidirectional and the products cannot be released back to free dormin. So once conjugated or oxidized, dormin is lost to it receptors and can no longer elicit physiological responses.
Transport of dormin is also functional and follows the vascular system. You can see that dormin formed in roots in the soil is transported via the xylem into the cells of the leaf. When the leaf is in water stress the evaporation of water decreases the H+ concentration in the mesophyll sap, raising the pH. So that in drought, the ABA arriving in the leaf is dissociated at its carboxylic acid group to ABA-. This charged form of ABA is not transported into the mesophyll cells and so it continues in transport to the guard cells where it does enter and causes stomatal closure. This is an appropriate response for drought conditions.
When rain finally arrives, the xylem is bringing lots of water in, increasing the H+ concentration, lowering the pH and the ABA is not dissociated. The uncharged ABA is absorbed into mesophyll cells as it it transported, and very little arrives at guard cells. So the stomata remain open. This is an appropriate response for well-watered conditions.
This response can be shown graphically below.
These diagrams show one of the major roles for dormin too. They demonstrate that water stress stimulates the uptake of dormin by the guard cells. This causes osmotic changes and stomatal closure. So dormin plays a major role in water stress physiology.
The dormin effect is upon membrane polarity and release of calcium into the cytosol...which leads to stomatal closure.
You might also remember our previous discussion of stomatal physiology in connection with blue-light responses. The figure below is for recall purposes dealing with proton pumping in guard cell protoplasts.
The proton pumping response is increased when ABA is present...again this leads to calcium pumping, reduced potassium pumping, and closure of the stomata. The relationship between dose of AbA and proton efflux is shown below.
While your book focuses on the role of dormin in stomatal closure, the chemical is known to influence other responses as well. As with the other hormones, this one is pleiotropic too. Dormin accumulates in seeds, promoting the desiccation tolerance of the embryo. It is associated with the accumulation of seed storage protein. It makes embryos dormant. Its breakdown during stratification and vernalization permits seed germination in many wild seeds. Its effect in that regard is antagonized by GA, which shares the biosynthetic pathway in part. Dormin accumulates in the summer buds of plants that will ultimately over-winter. This accumulation apparently results in the growth of leaf primordia into leathery bud scales and dormancy of the meristem inside these scales. Again, through the winter/spring process the dormin is oxidized and the bud breaks out of dormancy to produce a branch.