Development of Escherichia coli virus T1: repression of host gene expression.
Host protein synthesis, measured either as amino acid incorporation into proteins or as enzyme synthesis, is inhibited rapidly after infection Escherichia coli with T1. Analysis of this inhibition, using a technique which distinguishes between translation and transcription, revealed that translation of host mRNA is specifically blocked. Comparison of the time course of T1-induced host repression with inhibition by the drugs rifampicin, nitrofurantoin and chloramphenicol showed that T1 affects the initiation step of host translation. Intact membranes are apparently essential for host repression, suggesting a membrane-mediated process. Concomitant viral protein synthesis is not required. The membrane-altering principle is a constituent of the viral particle.
D001426:Bacterial Proteins / Q000096:biosynthesis / Q000235:genetics*; D002474:Cell-Free System; D003090:Coliphages / Q000254:growth & development*; D004926:Escherichia coli / Q000235:genetics* / Q000254:growth & development; D005690:Galactose; D010770:Phosphotransferases / Q000378:metabolism; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000235:genetics; D013997:Time Factors; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication; D001616:beta-Galactosidase / Q000378:metabolism
D001426:Bacterial Proteins; D012333:RNA, Messenger; D014764:Viral Proteins; D010770:Phosphotransferases; D001616:beta-Galactosidase; D005690:Galactose