Abstract
The development of the autophagic vacuole in P. berghei treated in the mouse host with chloroquine was studied using inhibitors of nucleic acid and protein synthesis. None of these inhibitors was capable of inducing an autophagic vacuole when administered alone. Inhibitors of ribosomal protein synthesis were maximally effective in halting autophagic vacuole formation due to chloroquine. Inhibitors of nucleic acid synthesis had delayed and incomplete effects. It was concluded that active synthesis of protein was necessary for the formation of the autophagic vacuole, and this organelle probably did not form as a result of a lesion in protein or nucleic acid synthesis.
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