Roles of AtTPC1, vacuolar two pore channel 1, in arabidopsis stomatal closure

Abstract

Abscisic acid (ABA) induces production of reactive oxygen species (ROS) and nitric oxide (NO), elevation of the cytosolic free calcium ion concentration ([Ca2]cyt) and cytosolic pH (pHcyt), and activation of S-type anion channels in guard cells, causing stomatal closure. To investigate whether Arabidopsis Two pore channel 1 (AtTPC1) that encodes the slow vacuolar (SV) channel is involved in stomatal closure, we examined stomatal movements and mobilization of second messengers in the attpc1-2 loss-of-function mutant in response to ABA, methyl jasmonate (MeJA) and Ca2. Both ABA and MeJA elicited production of ROS and NO, [Ca2]cyt oscillations, cytosolic alkalization and activation of S-type anion channel currents to lead to stomatal closure in the attpc1-2 mutant as well as the wild type. Unlike the wild type, in the attpc1-2 mutant exogenous Ca2 neither induced stomatal closure nor activated plasma membrane S-type anion channel currents despite [Ca 2]cyt elevation. These results indicate that AtTPC1 functions in response to external Ca2 but not to ABA and MeJA in Arabidopsis guard cells and suggest that AtTPC1 could be involved in priming of plasma membrane S-type anion channels by external Ca2 in Arabidopsis guard cells.