“…Simplified schematic model for Ca 2+ -specificity mechanism within ABA-dependent SLAC1 activation in guard cells. (A) Without ABA, Ca 2+ elevations that can also function in stomatal opening responses (Irving et al, 1992;Shimazaki et al, 1992;Curvetto et al, 1994;Shimazaki et al, 1997;Cousson and Vavasseur, 1998;Young et al, 2006) and spontaneous or un-specifically induced Ca 2+ transients (Allen et al, 1999b;Klüsener et al, 2002;Young et al, 2006;Yang et al, 2008;Siegel et al, 2009) do not lead to S-type anion channel (SLAC1) activation as PP2C protein phosphatases directly negatively regulate SLAC1 activation. (B) In the presence of ABA this SLAC1 inhibition is released, OST1 and CPKs phosphorylate, and thereby activate the channel.…”