Suppression of erythromycin resistance in ery-M1 mutants of Chlamydomonas reinhardi

Summary After mutagenesis of the erythromycin-resistant Chlamydomonas reinhardi strain ery-M1b, four mutants were isolated, each more sensitive to erythromycin than ery-M1b. All four mutants carry the original ery-M1b mutation which confers resistance and a separate mutation (es) which partially suppresses resistance. The mutants are designated es5ery-M1b, es101ery-M1b, es105ery-M1b, and es115ery-M1b. The suppressor mutations represent at least three different Mendelian loci. The suppressor es101 is located on the same linkage group as ery-M1, while the other suppressors are not linked to ery-M1.Although some of these suppressors can also mask the erythromycin resistance of ery-M2 strains, none had any effect on the non-Mendelian mutant ery-Ula. In addition, each suppressor affected the cross-resistance of ery-M1 mutants to other antibiotics. At least two of the changes in cross-resistance are due solely to the suppressor.Chloroplast ribosomes from cells carrying es5ery-M1b, es101ery-M1b, and es115ery-M1b have a greater affinity for ¹⁴C-erythromycin in vitro than those from ery-M1b. The degree of affinity depends upon the concentration of KCl.Each of these Mendelian suppressors probably affects a chloroplast ribosome function. Hence, a number of nuclear genes must play roles in the biogenesis of the chloroplast ribosome in Chlamydomonas reinhardi.