Transcriptional control of T4 coliphage-specific genes 30, 42, 43, rIIA, rIIB, and e.
Escherichia coli B/r (suo) was infected, at 30 degrees C, with T4Dam+, T4DamB24-amN82 (I-, 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: (I) All of the genes studied were transcribed exlusively 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.
D000818:Animals; D000956:Antigens, Viral; D002701:Chloramphenicol / Q000494:pharmacology; D003090:Coliphages / Q000378:metabolism*; D004254:DNA Nucleotidyltransferases / Q000096:biosynthesis*; D004279:DNA, Viral / Q000096:biosynthesis; D004285:Dogs; D010450:Endopeptidases / Q000096:biosynthesis*; D005796:Genes; D009154:Mutation; D011118:Polynucleotide Ligases / Q000096:biosynthesis*; D012293:Rifampin / Q000494:pharmacology; D013696:Temperature; D014158:Transcription, Genetic; D014166:Transferases / Q000096:biosynthesis*; D014170:Transformation, Genetic; D014764:Viral Proteins / Q000096:biosynthesis*
D000956:Antigens, Viral; D004279:DNA, Viral; D014764:Viral Proteins; D002701:Chloramphenicol; D014166:Transferases; D004254:DNA Nucleotidyltransferases; D010450:Endopeptidases; D011118:Polynucleotide Ligases; D012293:Rifampin