Physical mapping and cloning of bacteriophage T4 anti-restriction endonuclease gene.
We have proposed that the ability of T4 to produce non-glucosylated progeny after a single cycle of growth on a galU rglA rglB+ mutant of Escherichia coli is due to the initiation of the rglB+ function by a phage-coded, anti-restriction endonuclease protein. Based on this hypothesis, we screened T4 deletion mutants for failure to give a burst in this host. The absence of an arn gene in phage mutants lacking the 55.5- to 58.4-kilobase region is verified by their inability to protect secondary infecting non-glucosylated phage from rglB-controlled cleavage. A functional arn gene was cloned on plasmid pBR325, and the 0.8-kilobase insert DNA was shown to be homologous to the DNA missing in the arn deletion phage.
D003001:Cloning, Molecular; D004261:DNA Replication; D004262:DNA Restriction Enzymes / Q000037:antagonists & inhibitors*; D004279:DNA, Viral / Q000378:metabolism; D005814:Genes, Viral; D009154:Mutation; D013604:T-Phages / Q000235:genetics* / Q000254:growth & development; D014764:Viral Proteins / Q000235:genetics*; D014779:Virus Replication
D004279:DNA, Viral; D014764:Viral Proteins; C019077:anti-restriction proteins; D004262:DNA Restriction Enzymes