Abstract

Ten toxin and, to a lesser extent, dihydrotentoxin (both at lOmmol m~3) reduce stomatal opening in epidermal strips of Commelina communis in the light but not in darkness. This effect was significantly greater in normal air than in C02-free air. Fusicoccin overcame the tentoxin effect. However, tentoxin did not inhibit stomatal opening in the light in epidermal strips of Paphiopedilum harrisianum, a species which lacks guard cell chloroplasts. It is concluded that tentoxin exerts its action on stomata not by an ionophorous effect in the plasmalemma of guard cells but by the inhibition of photophosphorylation in their chloroplasts. The effects of DCMU and tentoxin on guard cells are discussed in terms of their effects on chloroplasts and the extent to which energy is supplied from this organelle during stomatal opening in the light. The results indicate that neither photophosphorylation nor non-cyclic electron transport in guard cell chloroplasts are essential for stomatal opening.

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