Abstract

Basal level synthesis of glutamine synthetase in the embryonic chick neural retina is mediated by labile, continuously supplied RNA templates. Complete blocking of protein synthesis with a high dose of cycloheximide does not prevent the transcription of these templates and allows their conservation and accumulation. When cycloheximide is withdrawn and, simultaneously, all further transcription is blocked, the accured templates are expressed. This results in synthesis and accumulation of glutamine synthetase at a faster than basal rate as determined by radio-immunochemical measurements. Puromycin, an inhibitor of translation with a different mechanism of action from cycloheximide, does not cause conservation of these templates. This, and studies at the polysomal level, indicate that template conservation by cycloheximide in this system depends on the specific mechanism by which cycloheximide inhibits translation.

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