Transcription Termination and Regulation in Bacteriophages P22 and Lambda

Abstract

INTRODUCTION
Evidence is accumulating indicating that control of the termination of transcription by specific protein effectors is an important mechanism of genetic regulation in bacteria and bacteriophages. The N-gene product of bacteriophage λ appears to stimulate expression of the “early” phage genes by preventing termination of transcription at sites that occur beyond the first gene of each of the early phage operons (Roberts 1969; Adhya, Gottesman and de Crombrugghe 1974; Franklin 1974). It has been suggested that the mechanism by which the Q-gene product of λ exerts its positive regulatory effect on the late genes also involves interference with termination of transcription (Roberts 1975; Sklar, Yot and Weissman 1975; Blattner and Dahlberg 1972). Finally, a similar control mechanism appears to regulate the expression of the tryptophan operon of E. coli: most transcription initiated at the trp promoter appears to be aborted at a site prior to the first structural gene unless termination is prevented through intervention of a control system that somehow senses starvation for tryptophan (Bertrand et al. 1975). In the case of the bacteriophages, and presumably in the case of the trp operon as well, protein regulators are implicated that are thought to interact with target sequences (in DNA or RNA) near a specific promoter to make transcription therefrom privileged against termination (Adhya, Gottesman and de Crombrugghe 1974; Franklin 1974).

Control by “antitermination” in phage λ was inferred primarily from the observation that the phage promoters are in most cases followed quite closely by transcription termination sites: transcription...