Previous studies with haploid erythromycin-resistant mutants mapping to the Mendelian locus ery-M1 in Chlamydomonas reinhardi have revealed the presence of an altered chloroplast ribosomal protein (LC6) (Mets and Bogorad, 1971, 1972;Davidson et al., 1974). Vegetative diploids of C. reinhardi heterozygous at the ery-M1 locus have now been constructed. Chloroplast ribosomes from such diploids contain 60-70% wild-type form of protein LC6 and 30-40% altered form of LC6. Growth assays show that these diploids are partially resistant to erythromycin. Whether the diploids are grown in the presence or absence of erythromycin, the same ratio of wild-type : altered form of LC6 in chloroplast ribosomes is observed. Therefore, resistant chloroplast ribosomes must be able to carry out protein synthesis even when many of the sensitive chloroplast ribosomes are blocked by erythromycin.
The presence of both the altered and wild-type forms of LC6 in diploids heterozygous at the ery-M1
locus is further evidence that a nuclear gene codes directly for a chloroplast ribosomal protein.
ations in a single chloroplast ribosomal protein (LC6) (Davidson et al., 1974). The work described above has provided evidence that locus ery-M1 is the site of the structural gene for chloroplast ribosomal protein LC6. We have now performed complementation analyses of the ery-M1
mutants in order to obtain additional information concerning the nature of the ery-M1 locus.
Diploids heterozygous for erythromycin resistance can also supply information on the mechanism of antibiotic inhibition of protein synthesis (Davis et al., 1975). Bacterial merodiploids heterozygous for erythromycin resistance have been reported to be antibiotic-sensitive (Nomura and Engbaek, 1972). We measured the degree of erythromycin sensitivity of C. reinhardi heterozygous diploids, wild-type, and haploid ery-M 1 mutants to determine whether sensitivity is dominant in diploids heterozygous for genes specifying chloroplast ribosome resistance.