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Transcriptional Control of T4 Coliphage-Specific Genes 30, 42, 43, rIIA, rIIB, and e

Department of Biological Sciences, University of Illinois at Chicago Circle, P.O. Box 4348, Chicago, Illinois 60680, U.S.A.

Escherichia coli B/r (su⁰) was infected, at 30 °C, with T4Dam⁺, T4DamB24amN82 (1^-, 44^-, DNA-negative phenotype), and T4DamN134amBL292 (33^-, 55^-, maturation-defective phenotype). A genetic (‘transformation’) assay was used to monitor transcription of genes 30 (polynucleotide ligase), 42 (deoxycytidylate hydroxymethylase), 43 (DNA polymerase), rIIA, rIIB, and e (endolysin). The principal results are: (1) All of the genes studied were transcribed exclusively from the so-called l-strand of phage DNA. (2) DNA synthesis and the maturation-defective proteins were required to turn-off transcription of genes 42, rIIA, tIIB, and 43. Experiments performed with chloramphenicol suggested that all phage-specific proteins required to turn-off transcription of these genes were not present until 6 to 8 min post infection (p.i.). (3) During a normal developmental programme, gene 30 was transcribed throughout the eclipse. DNA-negative and maturation-defective conditions had no obvious effect on transcription of this gene. (4) During a normal lytic event, two discrete waves of gene e transcription were observed. The late wave was dependent upon DNA-synthesis and presence of functional maturation-defective proteins. The early wave was unaffected by DNA-negative or maturation-defective conditions. Experiments with chloramphenicol indicated that, if any virus-specific proteins are involved with regulation of early e transcription, such proteins are present by 3 min p.i.

The data are interpreted to mean that early gene transcription is regulated by a minimum of two mechanisms. One of these mechanisms is fully operational by the 3rd min and, among the genes studied, controlled early e transcription. A second mechanism becomes operational between 6 and 8 min p.i. and controls transcription of genes 42, 43, rIIA, and rIIB.

^* Present address: Division of Virology, G. D. Searle & Co., Chicago, Illinois, U.S.A.

Received 15 July 1975; accepted 19 January 1976.