Diphtheria toxin resistance in Chinese hamster cells: genetic and biochemical characteristics of the mutants affected in protein synthesis.
Diphtheria toxin (DT) resistant mutants (Dipr) have been isolated from a number of different Chinese hamster lines. Among mutants affected in protein synthesis (DiprII class), two distinct phenotypes have been identified. In one class, the entire elongation factor-2 (EF-2) activity becomes resistant to DT-catalyzed ADP-ribosylation (DiprIIa class); these mutants behave recessively upon hybridization with sensitive cells. The second kind of protein synthesis mutants contain nearly normal levels of the ADP-ribosylatable EF-2 activity (DiprIIb class). The hybrids the two types of protein synthesis mutants complement each other indicating that mutations in different genes are responsible for them. While the DiprIIa class of mutants are presumably affected in the EF-2, the lesion in DiprIIb mutants seems to have occurred in a yet unidentified protein synthesis factor. Interesting differences are also observed in the characteristics of mutants that presumably are defective in the entry of toxin into cells (DiprI class).
D000246:Adenosine Diphosphate Ribose / Q000378:metabolism; D002460:Cell Line; D002463:Cell Membrane Permeability; D002474:Cell-Free System; D004167:Diphtheria Toxin / Q000494:pharmacology*; D004351:Drug Resistance; D006822:Hybrid Cells / Q000187:drug effects; D009154:Mutation; D010445:Peptide Elongation Factors / Q000378:metabolism*; D010641:Phenotype; D014176:Protein Biosynthesis
D004167:Diphtheria Toxin; D010445:Peptide Elongation Factors; D000246:Adenosine Diphosphate Ribose