%0 Journal Article %1 levchenko2005cytosolic %A Levchenko, V. %A Konrad, K. R. %A Dietrich, P. %A Roelfsema, M. R. G. %A Hedrich, R. %D 2005 %J Proceedings of the National Academy of Sciences of the United States of America %K Vicia-faba anion-channel ca2+-signals guard-cell s-type %N 11 %P 4203-4208 %R 10.1073/pnas.0500146102 %T Cytosolic abscisic acid activates guard cell anion channels without preceding Ca2+ signals %U http://www.pnas.org/content/102/11/4203.full.pdf?sid=b6ab7dcc-56ed-4da7-9028-0f3d08ab925c %V 102 %X 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.

@article{levchenko2005cytosolic, 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.}, added-at = {2017-05-23T15:29:07.000+0200}, author = {Levchenko, V. and Konrad, K. R. and Dietrich, P. and Roelfsema, M. R. G. and Hedrich, R.}, biburl = {https://www.bibsonomy.org/bibtex/23106a2bef8818779dc60a6fdd6dd661f/robroelfsema}, doi = {10.1073/pnas.0500146102}, interhash = {ab2b1be9b683c5f0f66a0d01b87f12f4}, intrahash = {3106a2bef8818779dc60a6fdd6dd661f}, issn = {00278424}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, keywords = {Vicia-faba anion-channel ca2+-signals guard-cell s-type}, number = 11, pages = {4203-4208}, refid = {20}, timestamp = {2017-05-23T15:33:56.000+0200}, title = {Cytosolic abscisic acid activates guard cell anion channels without preceding Ca2+ signals}, url = {http://www.pnas.org/content/102/11/4203.full.pdf?sid=b6ab7dcc-56ed-4da7-9028-0f3d08ab925c}, volume = 102, year = 2005 }