Functional inactivation of bacteriophage λ morphogenetic gene mRNA

THE synthesis of the morphogenetic proteins of bacteriophage λ seems to be regulated at the post-transcriptional level. This conclusion is based on the observation that the ratio of protein to DNA along the left arm of the λ genome varies from gene to gene by as much as 870-fold (Fig. 1), while the ratio of mRNA to DNA in this region varies less than twofold 1 , reflecting its transcription from a single promoter as a polycistronic mRNA 2–5 . These large variations in the molar ratios of the morphogenetic proteins could be explained by three different control mechanisms. (1) The initiation of protein synthesis could be controlled at the level of ribosome binding either by initiation factor complexes or by mRNA secondary structure 6,7 . (2) Some morphogenetic proteins could act to regulate their own translation or that of neighbouring genes (N. Sternberg, personal communication). (3) The differential translation of the late gene transcripts could be achieved by selectively inactivating some transcripts but not others. Our previous experiments using RNA:DNA hybridisation ruled out differential chemical decay of the mRNA derived from the late region of the genome, but did not exclude the possibility that differential functional inactivation of morphogenetic gene transcripts could account for the late protein to DNA variation 1 . Recent experiments indicate that functional and chemical decay are different processes which can vary widely in rate 8 and temperature dependence 9 . Functional decay in a polycistronic message generally seems to involve an endonucleolytic attack near the 5′-end of each gene transcript 8,10 at a specific target either in or near the ribosome-binding site 11 . Thus mRNA inactivation is not primarily a function of the length of a transcript and can vary from transcript to transcript within the same cell 11 . Because of this variation, differential functional decay has been invoked as a possibly significant mechanism of post-transcriptional control 11,12 .