CO 2 signaling in guard cells: Calcium sensitivity response modulation, a Ca 2+ -independent phase, and CO 2 insensitivity of the gca2 mutant

Abstract

Leaf stomata close in response to high carbon dioxide levels and open at low CO 2 . CO 2 concentrations in leaves are altered by daily dark/light cycles, as well as the continuing rise in atmospheric CO 2 . Relative to abscisic acid and blue light signaling, little is known about the molecular, cellular, and genetic mechanisms of CO 2 signaling in guard cells. Interestingly, we report that repetitive Ca 2+ transients were observed during the stomatal opening stimulus, low [CO 2 ]. Furthermore, low/high [CO 2 ] transitions modulated the cytosolic Ca 2+ transient pattern in Arabidopsis guard cells (Landsberg erecta ). Inhibition of cytosolic Ca 2+ transients, achieved by loading guard cells with the calcium chelator 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′ -tetraacetic acid and not adding external Ca 2+ , attenuated both high CO 2 -induced stomatal closing and low CO 2 -induced stomatal opening, and also revealed a Ca 2+ -independent phase of the CO 2 response. Furthermore, the mutant, growth controlled by abscisic acid ( gca2 ) shows impairment in [CO 2 ] modulation of the cytosolic Ca 2+ transient rate and strong impairment in high CO 2 -induced stomatal closing. Our findings provide insights into guard cell CO 2 signaling mechanisms, reveal Ca 2+ -independent events, and demonstrate that calcium elevations can participate in opposed signaling events during stomatal opening and closing. A model is proposed in which CO 2 concentrations prime Ca 2+ sensors, which could mediate specificity in Ca 2+ signaling.