Summary
Cycloheximide-resistant mutants of Physarum polycephalum were induced in the haploid myxamoebae by the combined action of UV1 and caffeine (Haugli and Dove, 1972) or by treatment with NMG2. Eight independent mutants segregated in a Mendelian fashion (Table 1). Crosses between 6 of the mutants revealed 2 loci, actA and actB, for cycloheximide resistance (Table 2).
All mutants are expressed in the plasmodium and are recessive in heterozygotes (Fig. 1 and 2). One mutation, conferring resistance to high levels of cycloheximide, was studied in heterokaryons and found to be incompletely recessive.
An in vitro peptide synthesizing system was constructed from ribosomes from Physarum and supernatant factors from Saccharomyces cerevisiae. Cycloheximide strongly inhibited the activity of ribosomes derived from either wild type or mutants at the actB locus. In contrast, ribosomes from mutants at the actA locus were resistant to cycloheximide. Thus, the actA locus operates through the ribosomes.
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Haugli, F.B., Dove, W.F. & Jimenez, A. Genetics and biochemistry of cycloheximide resistance in Physarum polycephalum . Molec. Gen. Genet. 118, 97–107 (1972). https://doi.org/10.1007/BF00267081
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DOI: https://doi.org/10.1007/BF00267081