Abstract
The phytohormone abscisic acid (ABA) reports on the water status
of the plant and induces stomatal closure. Guard cell anion channels
play a central role in this response, because they mediate
anion efflux, and in turn, cause a depolarization-induced K+
release. We recorded early steps in ABA signaling, introducing
multibarreled microelectrodes in guard cells of intact plants. Upon
external ABA treatment, anion channels transiently activated after
a lag phase of +/-2 min. As expected for a cytosolic ABA receptor,
iontophoretic ABA loading into the cytoplasm initiated a rise in
anion current without delay. These ABA responses could be elicited
repetitively at resting and at largely depolarized potentials (e.g., 0
mV), ruling out signal transduction by means of hyperpolarizationactivated
calcium channels. Likewise, ABA stimulation did not
induce a rise in the cytosolic free-calcium concentration. However,
the presence of +/-100 nM background Ca2+ was required for anion
channel function, because the action of ABA on anion channels was
repressed after loading of the Ca2+ chelator 1,2-bis(2-aminophenoxy)
ethane-N,N,N',N'-tetraacetate. The chain of events appears
very direct, because none of the tested putative ABA-signaling
intermediates (inositol 1,4,5 trisphosphate, inositol hexakisphosphate,
nicotinic acid adenine dinucleotide phosphate, and cyclic
ADP-ribose), could mimic ABA as anion channel activator. In patchclamp
experiments, cytosolic ABA also evoked anion current transients
carried by R- and S-type anion channels. The response was
dose-dependent with half-maximum activation at 2.6 uM ABA. Our
studies point to an ABA pathway initiated by ABA binding to a
cytosolic receptor that within seconds activates anion channels,
and in turn, leads to depolarization of the plasma membrane.
Users
Please
log in to take part in the discussion (add own reviews or comments).