Reversal of the Co₂‐responses of Stomata by Fusicoccin

S ummary The fungal toxin fusicoccin, which is known to stimulate stomatal opening, has been found to reverse the response of stomata to CO 2 . In the absence of fusicoccin, CO 2 caused stomata to close, while in its presence, CO 2 caused opening. This reversal of events was even more striking in epidermal malate levels. Three hundred and fifty μl l −1 CO 2 normally suppressed malate formation, but in the presence of fusicoccin, amounts of malate were greater in 350 μl l −1 CO 2 than in CO 2 ‐free air. These observations might be best explained if CO 2 exerts two different effects on guard cells, one of which is normally obscured by the other. The familiar effect, that of stomatal closure in response to increases in CO 2 concentration, is predominant, and it is suggested that this involves control of potassium ion uptake either through the activity of an electrogenic proton pump or through membrane permeability to K+. Fusicoccin has the effect of annulling this form of control by CO 2 , revealing an opposing response, namely a stimulation of opening by CO 2 . This could be due to a fixation of CO 2 into malate, which is used as a counter ion for K + in guard cells. There is, however, an enigma: the fact that (in the presence of fusicoccin) malate level is positively correlated with external CO 2 supply suggests that the latter limits the rate of malate formation, yet incorporation of labelled CO 2 can only account for about 1 % of the malate produced.