ABA signaling pathway... can anyone help me understand the order?

Question

I'm looking at how ABA stimulates stomatal closure, and I get that the exact mechanism is not known, but can anyone put all the various steps in the pathway in order, especially the part hydrogen peroxide plays? Either in words or a link to a good diagram, getting confused trying to put it all together from various papers.

Thanks Darren for a good answer, but looking for something a little more detailed and molecular biology orientated... any plant biologists?

Sorry, I meant Darrell...

Answer 1

I Dont know if this will be of any help but (im not a Biologist)

but it may or may not?

Water - protects against excessive water loss.
This is the prevailing and overriding control mechanism. There are two mechanisms by which water loss regulates stomatal closure, one of which is active and the other passive.

1. Hydropassive Control - simply put, as the plant looses water, the turgidity of the leaf cells, including guard cells, decreases and this results in stomatal closure. The plant is not "intentionally" closing the stoma, it is simply a consequence of drying out.
2. Hydroactive Control - this mechanism is one in which the plant actually seems to monitor its water status. When the water potential drops below some critical level, it engages a cascade of events that close the stomata. Presumably the plant is measuring pressure (turgor) and then synthesizes or releases an anti-transpirant that is translocated (moved) to the GC to cause closure.

http://employees.csbsju.edu/ssaupe/biol327/Lab/stomata/stomata-diagram.htm

The anti-transpirant is abscisic acid (ABA), one of the major plant growth regulators. It is active in very low concentration (10-6 M) and appears very rapidly after water stress (within 7 minutes). After 4-8 hours, the [ABA] increases nearly 50x. ABA comes from two sources: (a) root – in response to water stress, the xylem sap pH increases which in turn stimulates the release of ABA into the xylem sap for transport to the leaves. This seems to be a root signal to the leaves that "water stress is coming"; and (b) leaves – water stress stimulates a synthesis of new ABA and redistribution of existing ABA.

Mechanism of Action:
Treatment with ABA results in decrease of potassium, chloride and malate levels in the guard cells which in turn increase the water potential resulting in water efflux. Evidence suggests that there is an ABA receptor in the cell membrane. The receptor: (a) activates calcium channels in the membrane causing calcium uptake from the apoplast; (b) activates calcium channels in the tonoplast causing calcium release from the vacuole into the cytosol; (c) activates chloride (and malate) efflux channels; (d) inactivates potassium ion "in" channels; (e) inactivates the cell membrane proton pump; and (f) causes an increase in pH that activates potassium efflux channels. Thus, in short, ABA treatment causes an increase in cellular calcium levels which in turn results in decreases potassium and chloride levels and turns off the proton pump.