Effect of anisomycin on the cellular level of native ribosomal subunits

Treatment of Ehrlich ascites cells with anisomycin induces an almost threefold increase in the level of native 60S ribosomal subunits. This increase is not the result of an increase in rate of synthesis or transport of these subunits but is caused by a defect in the joining of the 60S subunits to the smaller initiation complex to form an 80S complex. Experimental evidence for such a blocking of the "joining reaction" could be found in the formation of "half-mer"-type oligosomes and by the release of extra 40S subunits when these oligosomes were treated with ribonuclease. Cycloheximide, an inhibitor of the translocation reaction, and inhibitors of the initiation prevent the increase of native 60S subunits induced by anisomycin. Our results imply that the increse of 60S subunits induced by anisomycin may be helpful in estimating the amount of initiating mRNAs in the cell.