Abstract: | Chlamydomonas reinhardii cells were treated with 5-fluorodeoxyuridine and ethylmethanesulfonate to induce mutagenesis. The mutant cells were analyzed for resistance against metribuzin (4-amino-6-(t-butyl)-3-methylthio-1,2,4-triazine-5-one). Clones with normal growth were isolated and the mutant cells further characterized. The photosynthetic rates of the mutant cells were about 20% lower than those of wild-type cells. The mutant cells were not only resistant against metribuzin (pI50 lowered from 6.65 to 3.41) but also against bromacil, atrazine, phenisopham and tolerant against 3-(3,4-dichlorophenyl)-1,1-dimethylurea. However, the mutant was more susceptible to phenolic electron-transport inhibitors like bromonitrothymol, ioxynil and i-dinoseb. 2,4-Dinitrophenyl-2′-iodo-3′-methyl-4′-nitro-6′-isopropyl phenyl ether inhibited the wild-type thylakoids more than the mutant. The analysis of the electron transport with artificial electron donors and acceptors showed that only Photosystem II was affected by the mutation and not Photosystem I. Binding experiments with isolated thylakoids of resistant and susceptible cells using 14C]metribuzin and 3H]-i-dinoseb revealed that metribuzin did not bind specifically to the thylakoids of the mutant cells, but that i-dinoseb did bind to the thylakoids of the mutant, and even better than to the thylakoids of the wild-type cells. Fluorescence studies confirmed these results. |