Abstract
The stomata of Commelina communis showed reduced opening responses to light and low C02 concentrations during the night phase of their entrained circadian rhythm. Increased supplies of potassium ions, and treatments with indol-3-ylacetic acid and fusicoccin, failed to promote opening during the night phase to a level equivalent to that in the day phase. The inability of fusiccocin to overcome the suppression of opening during the night phase contrasts with its ability to counteract the closure induced by agents such as C02, darkness and abscisic acid. It is concluded that there are at least two basic mechanisms by which the turgor of guard cells can be regulated, one which is susceptible to overriding control by fusicoccin and another which is unaffected by fusicoccin. Several previous studies had shown a positive correlation between malate in the epidermis (mainly located in guard cells) and stomatal opening. In the present experiments the aperture/malate correlation was broken in epidermis treated with fusicoccin during the night phase of the rhythm. The amount of malate present exceeded that associated with the same stomatal aperture in the day phase. Possible explanations are (1) that fusicoccin stimulates similar proton fluxes out of the guard cells during both phases of the rhythm, but an unknown factor imposes a restriction on stomatal opening during the night phase; (2) that there are lower proton fluxes in the night phase (limited, for example, by a reduced supply of ATP) but chloride availability or transport is reduced to an even greater extent so that a larger production of malate in the guard cells is required.
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