Repression of ant synthesis early in the lytic cycle of phage P22.
Using SDS-polyacrylamide gel electrophoresis to study the early expression of P22 genes we show that early expression of the ant-gene (imm I region) is turned off after 6-8 min, independent of the 'late' acting mnt-repressor. A semi-clear mutant called cir5 is defective for this early ant turn-off. The mutation cir5 maps in the imm I region of P22 between genes mnt and ant. P22 cir5 mutants are defective for a repressor which acts in trans to regulate early ant synthesis. There appears to be no absolute requirement of the cir5 allele for the establishment of lysogeny. The overproduction of ant in the P22 cir5 mutant leads to a marked increase in abortive infections, killing the infected cells. The cir5-phenotype can be suppressed by an ant- mutation.
D005786:Gene Expression Regulation; D005809:Genes, Regulator; D005814:Genes, Viral; D005816:Genetic Complementation Test; D008242:Lysogeny; D011995:Recombination, Genetic; D012097:Repressor Proteins / Q000037:antagonists & inhibitors / Q000235:genetics*; D012483:Salmonella Phages / Q000235:genetics* / Q000254:growth & development; D014157:Transcription Factors / Q000235:genetics*; D014764:Viral Proteins / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D054334:Viral Regulatory and Accessory Proteins
D012097:Repressor Proteins; D014157:Transcription Factors; D014764:Viral Proteins; D054334:Viral Regulatory and Accessory Proteins; C016649:phage repressor proteins