In , the expression of the phenylalanine biosynthetic operon is regulated by an attenuation mechanism. In the presence of excess phenylalanine, gene expression was decreased to 10% of the fully deattenuated level. To understand the factors that determine the basal level of expression, we examined the role of ribosome release from the leader peptide stop codon UGA. The transcriptional readthrough from the attenuator decreased by over 2-fold in the presence of the defective release factor 2. However, a release factor 1 (UAG and UAA specific) mutation did not influence the basal level of expression. These results support the proposal that the release of translating ribosomes from the leader peptide stop codon in stem 2 of the attenuator plays a crucial role in determining the basal level of expression of this gene.


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