Carbon dioxide induces increases in guard cell cytosolic free calcium
Carbon dioxide induces increases in guard cell cytosolic free calcium
Webb, Alex A.R.; McAinsh, Martin R.; Mansfield, Terry A.; Hetherington, Alistair M.
1996-03-01 00:00:00
The hypothesis that increases in cytosolic free calcium ([Ca2+]i) are a component of the CO2 signal transduction pathway in stomatal guard cells of Commelina communis has been investigated. This hypothesis was tested using fura‐2 fluorescence ratio photometry to measure changes in guard cell [Ca2+]i in response to challenge with 700 µl l−1 CO2. Elevated CO2 induced increases in guard cell [Ca2+]i which were similar to those previously reported in response to abscisic acid. [Ca2+]i returned to resting values following removal of the CO2 and further application of CO2 resulted in a second increase in [Ca2+]i. This demonstrated that the CO2‐induced increases in [Ca2+]i were stimulus dependent. Removal of extracellular calcium both prevented the CO2‐induced increase in [Ca2+]i and inhibited the associated reduction in stomatal aperture. These data suggest that Ca2+ acts as a second messenger in the CO2 signal transduction pathway and that an increase in [Ca2+]i may be a requirement for the stomatal response to CO2.
http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.pngThe Plant JournalWileyhttp://www.deepdyve.com/lp/wiley/carbon-dioxide-induces-increases-in-guard-cell-cytosolic-free-calcium-H2B2tRgPFS
Carbon dioxide induces increases in guard cell cytosolic free calcium
The hypothesis that increases in cytosolic free calcium ([Ca2+]i) are a component of the CO2 signal transduction pathway in stomatal guard cells of Commelina communis has been investigated. This hypothesis was tested using fura‐2 fluorescence ratio photometry to measure changes in guard cell [Ca2+]i in response to challenge with 700 µl l−1 CO2. Elevated CO2 induced increases in guard cell [Ca2+]i which were similar to those previously reported in response to abscisic acid. [Ca2+]i returned to resting values following removal of the CO2 and further application of CO2 resulted in a second increase in [Ca2+]i. This demonstrated that the CO2‐induced increases in [Ca2+]i were stimulus dependent. Removal of extracellular calcium both prevented the CO2‐induced increase in [Ca2+]i and inhibited the associated reduction in stomatal aperture. These data suggest that Ca2+ acts as a second messenger in the CO2 signal transduction pathway and that an increase in [Ca2+]i may be a requirement for the stomatal response to CO2.
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