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Abstract

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In the light-dependent carotenoid synthesis in Fusarium aquaeductuum photoinduction can be substituted by incubation of the mycelium with the SH-group poisons p-chloro-and p-hydroxymercuribenzoate in the dark. The minimum concentration of both substances effective for induction is 5.10(-6) molar; maximal production of pigments occurs at molar concentration of 5.10(-5)-10(-4). In the mycelium incubated with mercuribenzoate, carotenoid synthesis starts after a lagperiod of 4-6 hours, increases until 24 hours after addition of the poison and then continues for some days at a constant rate. The result that the lag-period after treatment with mercuribenzoate is much longer than it is after photoinduction may be due to the fact that in the presence of mercuribenzoate the respiration of the mycelium is severely decreased (to 25% of the normal value at molar concentrations of 5.10(-5)) and as consequence other metabolic processes are also depressed. From experiments in which p-hydroxy-mercuribenzoate was removed at different times after addition by washing with distilled water, it can be seen that even an incubation time of only 2 hours is effective for induction. Other SH-group blocking substances do not induce carotenoid synthesis; other mercuring compounds and benzoic acid are also ineffective.Carotenoid production induced by illumination or by incubation with mercuri-benzoate is quantitatively inhibited by actidion (cycloheximid), which is a potent inhibitor of protein synthesis in fungi. The inhibition decreases with increasing time between the beginning of illumination or incubation with mercuribenzoate and the addition of actidion; from this result it can be concluded that as a consequence of the induction reaction carotenogenic enzymes are newly formed. If actidion is added 3 hours after the beginning of illumination there is almost no inhibition of pigment production, indicating that carotenoid synthesis itself is not inhibited by actidion.From these results it is concluded that light and mercuribenzoate may catalyse the same reaction in the chain of the regulatory mechanism, namely, a blocking of SH-groups. We therefore assume that the function of light in the induction mechanism is to photooxydize SH-groups of a specific compound. Several possibilities as to which compound may be the site of this reaction are discussed.

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