Postinfection control in T4 bacteriophage infection: inhibition of the rep function.
We suggest that the general mechanism by which T4 phage turns off host macromolecular synthesis involves specific phage proteins which react with key components in the synthetic pathway. Support for this mechanism exists for the inhibition of host RNA synthesis. Here we note that the host rep function was inhibited after T4 phage infection. Since rep functions are known to be involved in host DNA replication, inhibition of rep might alter the course of host DNA replication.
D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D002701:Chloramphenicol / Q000494:pharmacology; D004265:DNA Helicases / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D004790:Enzyme Induction; D004926:Escherichia coli / Q000201:enzymology; D029968:Escherichia coli Proteins; D013604:T-Phages / Q000502:physiology*; D014764:Viral Proteins / Q000096:biosynthesis
D029968:Escherichia coli Proteins; D014764:Viral Proteins; C506744:rep protein, E coli; D002701:Chloramphenicol; D000251:Adenosine Triphosphatases; D004265:DNA Helicases