Regulation of lambda rex expression after infection of Escherichia coli K by lambda bacteriophage.
The ability of Escherichia coli K to support bacteriophage T4rII replication starts to decline at 3 to 6 min after infection by lambda. This inhibition appears to depend on expression of the lambdarex(+) gene, since little inhibition was observed following infection by a lambdarex mutant or by a hybrid bacteriophage lambdai(434) which lacks a functional rex gene. For promotion of the synthesis of rex product, cII(+) and N(+) genes are required and can act trans, whereas cY(+), also required, must be cis to a rex(+) gene. These genes presumably play a role in the transcription of the cI-rex operon because they are also known to be required for repressor (cI product) synthesis. Functional cIII, O, P genes are not necessary for ample rex product synthesis. We also observed full rex expression after infection by lambdasuscI mutants, suggesting that rex and repressor are separate gene products and that repressor is not required for inhibition of T4rII replication. We also report experiments with a rex mutant that is not leaky when in a lysogen but is sufficiently leaky shortly after infection to cause inhibition of T4rII replication.
D002874:Chromosome Mapping; D003090:Coliphages / Q000254:growth & development*; D004926:Escherichia coli; D005809:Genes, Regulator; D005815:Genetic Code; D005816:Genetic Complementation Test; D006824:Hybridization, Genetic; D008242:Lysogeny; D009154:Mutation; D009876:Operon; D011995:Recombination, Genetic; D013997:Time Factors; D014779:Virus Replication