Control of gene expression in bacteriophage lambda: suppression of N mutants by mutations of the antirepressor.
The lysogenization and induction properties of phages lambdasusN7CI857Ai7 and lambdasusN53cro27 are described. Both phages, at 32 degrees kill little, but show only a moderate frequency of lysogenization whether an amber suppressor is present or absent in the host bacterium. In  the latter case, lysogens for lambdasusN7CI857Ai7 or lambdasusN53CI857cro27 can exist in two different regulatory states, here called P r- and Pr+. The Pr+ phase is characterized by phage release and cell death at 40 degrees; conversely, cells in the Pr- phase are similarly killed but release no or very little phage. Pr- is the phase usually obtained at lysogenization. Each phase may be transmitted at 32 degrees for an unlimited number of generations, however, shifts to the opposite phase take place from time to time with a low probability. Two previously described antirepressor defective mutants. Ai7 and cro27, were found to suppress specifically the growth defect caused by an amber mutation in gene N. This suppression is observed in non-suppressing hosts at 40 or 42 degrees. Apparent revertants of N- mutants were shown to be often (80%) caused by a second mutation, in the Ai gene (also called tof, cro and fed). All the revertants so far examined appeared to be recessive. Lambda phages bearing a double amber mutation in gene N did not acquire full N independence by the acquisiton of an Ai mutation; this could be achieved, however, in the presence of a CII mutation. The above findings are discussed in terms of a direct interaction between the N, Ai and CII products.
D003090:Coliphages / Q000378:metabolism*; D004926:Escherichia coli; D005809:Genes, Regulator; D008242:Lysogeny; D009154:Mutation; D010641:Phenotype; D014176:Protein Biosynthesis; D011995:Recombination, Genetic; D014764:Viral Proteins / Q000378:metabolism*
D014764:Viral Proteins