ABA Transport and Distribution in Relation to Its Function in Plants - Abscisic Acid: Metabolism, Transport and Signaling - page 64

transported from the chloroplast or vascular tissues to their sites of action in guard
cells. To reveal the mechanisms by which ABA mediates drought-induced stoma-
tal closure, it is imperative that we identify the sites of ABA action at the guard
cells. In the early 1980s, Hartung ( 1983 ) demonstrated that the primary site of
ABA action at the guard cell plasmalemma is either at the outer surface of the
plasmalemma or at another position that is readily accessible from the outside,
because exogenous ABA is able to induce stomatal closure at high pH (i.e., 8.0),
in the absence of ABA uptake. Given that Arabidopsis NCEDs and AAO3 are pri-
marily localized in vascular tissues, Seo and Koshiba ( 2011 ) proposed that water
shortages are first perceived by leaf vascular tissues and that the ABA signal origi-
nates from the vascular tissues that induce stomatal closure.
However, this hypothesis does not consider the roles of ABA in the chloroplasts
of mesophyll and guard cells. As mentioned above, ABA is abundant in both the
vascular tissues and chloroplasts. Furthermore, guard cells are not only directly
attached to mesophyll cells, but also themselves contain chloroplasts. Therefore,
the ABA in mesophyll and guard cells may also regulate stomatal movement.
Actually, most of the earlier works suggested that ABA in the mesophyll and
guard cells plays important roles in stomatal closure. Based on the anion-trap
mechanism for ABA, Hartung and Slovik ( 1991 ) developed a mathematical model
with which they analyzed the redistribution of ABA in relation to stomatal clo-
sure in leaves in response to drought stress. Based on their analysis, Hartung and
Slovik ( 1991 ) proposed that drought stress causes a pH shift in different compart-
ments of leaves and this pH shift induces a complicated redistribution of ABA
among compartments. The redistribution of ABA may cause ABA to accumu-
late in guard cell walls to levels that are more than 16-fold over the initial value,
which would be sufficient to induce stomatal closure. Furthermore, these authors
proposed that it is the plasmalemma of the epidermal cells that initially senses
drought stress, such that the epidermal cells play an important role in triggering
stomatal closure, and the mesophyll cells function to support stomatal closure
only synergistically. By quantifying the amount of ()-3H-ABA released from
()-3H-ABA-loaded Xanthium leaves, Bray and Zeevaart ( 1985 ) demonstrated
that the efflux of endogenous ABA from cells was indeed closely correlated with
the pH gradients among the various cellular compartments, and moreover that
this efflux could be promoted by drought stress. In agreement with Hartung and
Slovik's proposal described above, immunogold localization analysis in lavender
leaves showed a fourfold increase in ABA, as reflected by the density of immu-
nolabeling in the cell wall under drought (Pastor et al. 1998). Furthermore, Wang
and Jia ( 1995 ) used immunogold electron microscopy localization to show that
drought stress could lead to an evident increase in ABA content in the apoplast of
the epidermis, while ABA content in mesophyll cells remained constant during the
early stages of water stress. Interestingly, in response to drought stress, ABA was
found to preferentially accumulate in the dorsal wall of guard cells.
While drought stress-induced stomatal closure is generally thought to be medi-
ated by ABA coming from mesophyll and vascular cells, it is difficult to under-
stand why stomatal movement is not affected by the ABA in the mesophyll and