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REVERSAL OF THE CO 2 ‐RESPONSES OF STOMATA BY FUSICOCCIN
Author(s) -
Travis A. J.,
Mansfield T. A.
Publication year - 1979
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/j.1469-8137.1979.tb02292.x
Subject(s) - fusicoccin , guard cell , biophysics , potassium , biology , chemistry , botany , biochemistry , atpase , enzyme , organic chemistry
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.