The fungal toxin fusicoccin, which is known to stimulate stomatal opening, has been found to reverse the response of stomata to CO2. In the absence of fusicoccin, CO2 caused stomata to close, while in its presence, CO2 caused opening. This reversal of events was even more striking in epidermal malate levels. Three hundred and fifty μl l−1 CO2 normally suppressed malate formation, but in the presence of fusicoccin, amounts of malate were greater in 350 μl l−1 CO2 than in CO2-free air.

These observations might be best explained if CO2 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 CO2 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 CO2, revealing an opposing response, namely a stimulation of opening by CO2. This could be due to a fixation of CO2 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 CO2 supply suggests that the latter limits the rate of malate formation, yet incorporation of labelled CO2 can only account for about 1 % of the malate produced.