Abstract

Bacteriophage SPO1 host-dependent mutants in three cistrons show defects in the program of viral transcription (Gage & Geiduschek, 1971a). Mutants in two eistrons ( sus F4 and sus F14) are analogous to T4 maturation defective mutants: they replicate viral DNA in the non-permissive host but are unable to make viral late l or m 2 l, RNA and do not form protein subassemblies of the virion. These mutants are also unable to shut off viral m transcription. A mutant in a third cistron ( sus F21) only transcribes that viral RNA ( e, em) for which no protein synthesis in the infected cell is required. Non-permissive sus F21 infected cells fail to make m, m 1 l, or m 2 l, RNA and almost entirely cease viral transcription eight to ten minutes after infection (at 37 °C). These transcriptive defects suggest a simple hierarchical ordering of the normal temporal sequence of wild-type viral transcription. That ordering, in turn, suggests a model of transcription during viral development that involves not less than three control elements of viral transcription, two of which are positive and one of which is negative.

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