Figure 3. (Partially) hypothetical model of the signaling pathways leading to abscisic acid-mediated stomatal closure/inhibition of stomatal opening.

Figure 3

(Partially) hypothetical model of the signaling pathways leading to abscisic acid-mediated stomatal closure/inhibition of stomatal opening. Abscisic acid (ABA) is perceived by a receptor whose identity is still disputed, presumable at the cell surface. Downstream signaling from this receptor leads to increased LCB kinase activity and elevated levels of LCB-1-P. The LCB-1-P is perceived by a yet unknown receptor. Two possibilities can be envisaged in analogy to the situation in mammalian cells: Perception by an unknown intracellular receptor59 could be directly relayed to the release of calcium from intracellular stores, presumably the vacuole. Alternatively, LCB-1-P could be secreted and perceived by a membrane-bound receptor in an autocrine or paracrine fashion. This model is well established in mammalian cells20 and support for its validity in plants comes from the finding that the induction of stomatal closure by microinjection of LCB-1-P depends on the sole G-protein alpha-subunit encoded by the Arabidopsis genome, GPA160,61 Activated GPA1 would then induce downstream responses like calcium release, the opening of pH-dependent anion channels and the inhibition of inward rectifying potassium channels. Inhibition of the latter leads to loss of turgor followed by closing (or inhibition of opening) of the guard cells. GPA1 is negatively regulated by the G protein-coupled receptor protein GCR1.62 Solid arrows represent known interactions or ion currents, dashed arrows hypothetical or indirect interactions. Grey boxes represent proteins of unknown identity.

From: Biosynthesis of Sphingolipids in Plants (and Some of Their Functions)

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