In this and the following paper, expression of the phage T4 late genes in the absence of DNA replication has been examined. With only one exception, mutants that block viral replication allow synthesis of late RNA and late proteins. The peculiar character of the DNA replication-independent T4 late transcription (measured, in our experiments, as RNA that hybridizes with the isolated r-strand of T4 DNA) is the dependence of the proportion of r-transcription on the number of infecting phage and the temperature sensitivity of this transcription. Mutants in gene 45 fail to synthesize appreciable proportions of late RNA. The effects of mutations in gene 45 on late transcription are more severe than those in the other hitherto identified T4 late transcription control genes, 33 or 55. We conclude (see also the following paper by Wu et al., 1975) that the product of T4 gene 45 is required for T4 late transcription as well as for DNA replication. Mutants in four T4 DNA genes-30, 41, 46 and 56-have defective replication but synthesize some viral DNA. Mutations in three of these genes, 30, 41 and 46, allow the synthesis of T4 late RNA at levels that do not depend on the multiplicity of infection. Mutations in gene 56 (which codes for a dCTPase) lead to the synthesis of T4 DNA containing C in place of hydroxymethyl. Such DNA is subject to degradation by virus-specified endo- and exonucleases. In cells infected with a gene 56 mutant, some r-strand-specific T4 RNA is synthesized but synthesis of late T4 proteins is defective. We provide evidence that this is an intrinsic property of C-containing T4 DNA rather than a consequence of its susceptibility to degradation by phage-specified nucleases.
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