1. Treatment of wild-type cells of Chlamydomonas reinhardi with high concentrations of erythromycin results in increased recovery of membrane-bound chloroplast ribosomes, presumably by preventing polysomal runoff during harvesting of cells. No such membrane-retention effect is detected if erythromycin is added after harvesting of cultures, before cell breakage. 2. Growth of wild-type cells is inhibited by 10 microgram/ml erythromycin, but a concentration twice as high is required to increase recovery of membrane-bound wild-type ribosomes. On the other hand, the concentrations of erythromycin which inhibit growth of mutant ery-M1b produce a membrane-retention effect. Mutant ery-U1a is resistant to high concentrations of erythromycin and no membrane-retention effect is detectable at concentrations which produce one in wild type and ery-M1b. 3. These results can be reconciled by a two-point model of the mechanism of erythromycin action on chloroplast ribosomes in Chlamydomonas.
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