Three mutants of Scenesdesmus D3 designated 8, A′, and 26 by Dr. Norman Bishop, were compared with the wild type strain with respect to their ability to fix 14CO2 photosynthetically. Intact cells were also studied using the techniques of electron paramagnetic resonance (EPR) spectroscopy to identify the presence as well as the magnitude of the characteristic light-induced Signal I. Cell-free systems prepared from these same organisms were assayed for their competence to carry out photophosphorylation and photoreduction. The effect of several added co-factors in these systems was also studied including ferricyanide, phenazine methosulfate, ascorbic acid, and dichlorophenolindophenol (DCIP). Mutant 26 is able to carry out cyclic photophosphorylation, but is unable to photoreduce NADP+. It has a normal EPR Signal I, and the lesion appears to be in the flow of electrons between Photosystem I and the pyridine nucleotide. Mutant A′ is devoid of activity in Photosystem II. It is unable to carry out photoreduction unless electrons are provided from the DCIP-ascorbate couple. Mutant 8 is characterized by a unique ability to photoadapt its mutation. Mutant 8 cells grown in continuous light for approx. 30 days regain their photosynthetic ability and appear competent to carry out CO2 fixation, photoreduction and photophosphorylation. Photosystem I activity and Signal I, absent in dark-grown cells is present in the light-grown organism. When such cells are returned to the dark they gradually deadapt and resume their mutant biochemical behavior. By treating dark-grown Mutant 8 cells with heat and a detergent, Triton X-100, Signal I appears. These data localize the lesion in Mutant 8 in the flow of the electrons in Photosystem I. It is postulated that alterations in the micro environment of Photocenter I induced by detergent or by light permit the flow of electrons through Photocenter I. © 1969.
