Cytosolic abscisic acid activates guard cell anion channels without preceding Ca2+ signals.

Dietrich P (2005)


Publication Language: English

Publication Status: Published

Publication Type: Journal article, Original article

Publication year: 2005

Journal

Book Volume: 102

Pages Range: 4203-4208

Journal Issue: 11

DOI: 10.1073/pnas.0500146102

Open Access Link: http://www.pnas.org/content/102/11/4203.long?tab=author-info

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 approximately 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 hyperpolarization-activated calcium channels. Likewise, ABA stimulation did not induce a rise in the cytosolic free-calcium concentration. However, the presence of approximately 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 patch-clamp 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 microM 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.

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How to cite

APA:

Dietrich, P. (2005). Cytosolic abscisic acid activates guard cell anion channels without preceding Ca2+ signals. Proceedings of the National Academy of Sciences of the United States of America, 102(11), 4203-4208. https://dx.doi.org/10.1073/pnas.0500146102

MLA:

Dietrich, Petra. "Cytosolic abscisic acid activates guard cell anion channels without preceding Ca2+ signals." Proceedings of the National Academy of Sciences of the United States of America 102.11 (2005): 4203-4208.

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