Failure of translational repression in the phage f2 op3 mutant is not due to an altered coat protein-RNA interaction.
A secondary phenotype of the op3 mutant of RNA bacteriophage f2 is the absence of translational repression of the phage replicase gene by the phage coat protein. We have synthesized RNA fragments corresponding to the site of translational repression for both the wild type and the op3 mutant. Using a quantitative assay, we show that the affinity of the closely related R17 coat protein for the mutant and wild type RNA fragments is the same. In addition, we find that the op3 and R17 coat proteins bind to the wild type RNA fragment with essentially identical dissociation constants. Thus, the altered regulation of replicase protein synthesis in the op3 mutant does not appear to be due simply to a reduced affinity of the translational repressor for its target site.
D001435:Bacteriophages / Q000235:genetics*; D001483:Base Sequence; D009154:Mutation; D010641:Phenotype; D014176:Protein Biosynthesis; D012367:RNA, Viral / Q000378:metabolism*; D014759:Viral Envelope Proteins / Q000378:metabolism*
D012367:RNA, Viral; D014759:Viral Envelope Proteins