Rhythmic potassium flux in albizzia: effect of aminophylline, cations, and inhibitors of respiration and protein synthesis.
Rhythmic leaflet movement in Albizzia is controlled by rhythmic K(+) flux in pulvinal motor cells. The angle assumed by darkened leaflets during the open phase of the rhythm can be altered by various compounds and changes in temperature; such treatments are ineffective during the closed phase. In all cases, effects on leaflet angle are correlated with and probably a consequence of K(+) flux in pulvinal motor cells. Incubation at low temperature (6C) or on sodium azide (1.0 mm) reduces K(+) in the ventral motor region and increases K(+) in the dorsal motor region, thereby decreasing leaflet angle. Incubation on cycloheximide (0.1 mm) or sodium acetate (0.05 m) inhibits protein synthesis; if the incubation period immediately precedes the opening phase, these compounds prevent both K(+) flux into the ventral motor cells and leaflet opening. Magnesium nitrate (0.05 m), supplied after leaflets have started to open, promotes K(+) secretion from the dorsal motor cells and increases the angle of opening.The data support the following hypothesis. Active K(+) transport into the ventral motor cells and out of the dorsal motor cells leads to opening; K(+) leakage in the opposite directions causes closure; and the interaction of these processes results in a rhythmic oscillation. Proteins in the ventral cell membranes that are required for active transport or membrane integrity turn over rhythmically and are resynthesized before opening. The availability of divalent cations determines the phase relationships between the K(+) rhythms in the dorsal and ventral motor cells.White light phases the rhythm. The "light on" signal turns on a K(+) secreting pump in the dorsal motor cells, while the "light off" signal initiates a period of protein synthesis which in turn leads to active K(+) transport into the ventral motor cells. Aminophylline (0.1-6.0 mm) inhibits white light-promoted opening and nyctinastic closure.
Satter
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RL
Department of Biology, Yale University, New Haven, Connecticut 06520.
Applewhite
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PB
Galston
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AW