Ricinus communis toxin-mediated inhibition of protein synthesis in cell-free extracts of a toxin-resistant variant mouse lymphoma cell line.
Ricinus communis agglutinin II (RCAII, ricin, toxin) at low concentrations inhibits protein synthesis in cell-free extracts, but not in intact cells, of an RCAII-resistant mouse lymphoma variant cell line. The concentration dependence of the inhibition by RCAII was the same in cell-free extracts of both RCAII-resistant variant and RCAII-sensitive parental cells, while intact parental cells are 250 times more sensitive to RCAII toxicity. The onset of RCAII inhibition of cell-free protein synthesis was extremely rapid in both cases, being complete in a few minutes. Under these conditions RCAII inhibits protein synthesis in intact RCAII-sensitive parental cells, but maximal inhibition requires several hours to occur. These results support our previous electron microscopic observations that the variant cells are defective in the uptake of RCAII by endocytosis at low toxin concentrations.
D000818:Animals; D002460:Cell Line; D002474:Cell-Free System; D004351:Drug Resistance; D004705:Endocytosis; D014644:Genetic Variation; D008223:Lymphoma; D051379:Mice; D009363:Neoplasm Proteins / Q000096:biosynthesis*; D010940:Plant Proteins / Q000494:pharmacology*; D012276:Ricin / Q000378:metabolism / Q000494:pharmacology*
D009363:Neoplasm Proteins; D010940:Plant Proteins; D012276:Ricin