A Two-Ribosome Model for Attenuation

Abstract

The first insights into the mechanisms of gene regulation were provided by the work of François Jacob and Jacques Monod in early 1960s. The results of their elegant genetic studies concerning the regulation of the lactose utilization operon of Escherichia coli suggested the presence of a repressor molecule that acted in trans to repress the expression of the genes of the operon.^1,2 Later, Ellis Englesberg and his colleagues showed that trans-acting factors could affect gene expression in a positive manner as well.³ Subsequently, positive and negative trans-acting effectors of gene expression were demonstrated for many metabolic pathways in bacteria, bacteriophage, and eukaryotic organisms. In each of these systems, however, regulation was exerted at the level of transcription initiation. It was not until the late 1970s that Charles Yanofsky and his colleagues demonstrated a fundamentally different type of gene regulation. They showed that, in addition to regulation by repression, the genes of the tryptophan operon of E. coli are subject to regulation by transcription termination. The regulation of transcription termination at a site preceding the structural genes of an operon is called attenuation. Transcription attenuation is now recognized as a common mechanism for the regulation of gene expression in bacteria and more general forms of attenuation have been described in eukaryotic cells and their viruses (reviewed in refs. 4–6).