Transient activation of RNA polymerase in Escherichia coli B after infection with bacteriophage T4.
Sköld and Buchanan(1) have reported that there is a rapid loss of RNA polymerase activity in Escherichia coli B after infection with T4 bacteriophage. More recent studies on the mechanism of this inactivation have been made in this(2) and other laboratories.(3, 4) In this communication, we report the observation of a transient stimulation of RNA polymerase activity when measurement is made immediately after infection and when cells are ruptured by a gentle lysis procedure. The increase in activity is independent of the synthesis of protein. The activity in the extracts of infected cells is lost by treatment of the extract with antibody to E. coli RNA polymerase and is refractive to the inhibitory action of the antibiotic rifamycin. Hybridization experiments indicate that an RNA transcribed almost exclusively from a T4 DNA template is the product of incubation of extracts of infected cells with a reaction mixture containing an exogenous primer (salmon sperm DNA). These findings are consistent with the hypothesis that one of the first steps in phage infection is the formation of a transcription complex containing T4 DNA and E. coli RNA polymerase.
D000818:Animals; D003090:Coliphages; D004926:Escherichia coli / Q000201:enzymology*; D005815:Genetic Code; D006824:Hybridization, Genetic; D007239:Infections; D008297:Male; D012316:RNA Nucleotidyltransferases / Q000378:metabolism*; D012293:Rifampin / Q000494:pharmacology; D012487:Salmonidae; D013094:Spermatozoa; D013995:Time
D012316:RNA Nucleotidyltransferases; D012293:Rifampin