Effect of an antiserum to a thylakoid membrane polypeptide on the primary photoreaction of photosystem II.
As was described previously, an antiserum to polypeptide 11000 inhibited photosynthetic electron transport on the oxygen evolving side of photosystem II. The effect of the antiserum on chloroplasts from two tobacco mutants also clearly showed that the inhibition site is on the photosystem II-side of the electron transport chain. One of the two tobacco mutants lacks the oxygen evolving capacity but exhibits some electron transport with tetramethyl benzidine, an artificial donor to PS II. In this mutant electron transport was barely inhibited. The effect of the antiserum on the primary photoevents showed that the initial amplitude of the absorption change of chlorophyll aII at 690 nm and that of the primary electron acceptor X320 at 334 nm both diminished in the presence of the antiserum. Both signals were restored upon addition of diphenylcarbazide another artificial donor to photosystem II. Comparison of the degree of inhibition on the amplitudes of the fast and slow components of the 690 nm absorption change with the manometrically measured inhibition of electron transport shows that besides a full inactivation of a part of the reaction centers of photosystem II another part apparently mediates a fast cyclic electron flow around photosystem II as reported by Renger and Wolff earlier for tris-treated chloroplasts. Moreover, the antiserum affects the low temperature fluorescence in a way which is opposite to Murata's effect of the Mg2+-ion induced inhibition of energy spill-over from photosystem II to phytosystem I. The antiserum under the condition in which the Hill reaction is inhibited lowered the 686 nm emission and enhanced the 732 nm emission which indicates an enhanced energy spill-over to photosystem I.