THE ACTION OF FUSICOCCIN ON STOMATAL GUARD CELLS AND SUBSIDIARY CELLS

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<jats:title>SUMMARY</jats:title><jats:p>The fungal toxin, fusicoccin, induces wilting when applied to uninfected plant material. We have confirmed that fusicoccin stimulates stomatal opening and the entry of potassium into the guard cells. When detached epidermis of Commelina communis is placed in a potassium‐free medium containing 10 μM fusicoccin, the stomata open widely and potassium accumulates in the guard cells, demonstrating that sufficient endogenous potassium is available.</jats:p><jats:p>The failure of stomata to open on isolated epidermis is discussed. It is suggested that the subsidiary cells respond to a wound hormone produced after stripping off the epidermis, the effect of which is to block the normal route taken by potassium as it moves into the guard cells. A physiological role for the subsidiary cells in regulating stomatal movements is thus strongly indicated.</jats:p><jats:p>Fusicoccin is able to overcome the effect of those environmental factors, darkness and high CO<jats:sub>2</jats:sub> concentrations, which normally inhibit stomatal opening. Evidence is presented that, in this case, it must act within the guard cells and not only on the subsidiary cells. The time of exposure to the toxin required for a subsequent opening response of the stomata is very short. Stomata in contact with 10 μM fusicoccin for 1 min open almost as widely as those exposed to the same concentration for 2 h.</jats:p>

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