abstract
- The molecular basis of resistance to the protein synthesis inhibitor emetine has been examined in cell-free, protein-synthesizing extracts derived from normal and emetine-resistant (EmtR) mutants. We had earlier shown that protein synthesis in extracts of the mutant cells was resistant to the inhibitory action of emetin. When extracts from a wild-type and mutant cell line were fractionated into supernatant (S-100) and polyribosome fractions and mixed in different combinations, resistance to emetine was found to be associated with the mutant polyribosome fraction. Further fractionation of wild-type and mutant polyribosomes into 40S and 60S ribosomal subunits and mixing them in various combinations with an S-100 fraction from the wild-type cell indicates that resistance of mutant cells to emetine involves an alteration in the 40S ribosomal subunit. The behavior of EmtR has also been examined in somatic cell hybrids. Studies of EmtR X EmtS hybrid cell lines in vivo and in vitro show that EmtR is pheontypically recessive to EmtS, which is consistent with the ribosomal location of the genetic change.