Mechanism of araC autoregulation and the domains of two overlapping promoters, Pc and PBAD, in the L-arabinose regulatory region of Escherichia coli.

Abstract

The DNA-protein contact sites in the ara regulatory region, which contains the promoters for araBAD and araC, were determined for araC protein, the cAMP-binding protein and RNA polymerase by using the methylation protection and DNase I protection methods. The functional significance of binding was assessed by correlating the state of occupancy of these sites with promoter activity in transcription initiation. Results suggest that the basis for araC autoregulation is that araC protein, in either its activator (P2) or repressor (P1) form, acts as a repressor for araC, by binding to the RNA polymerase attachment site at the araC promoter. The araC and araBAD promoters share a common site of positive control by the cAMP-binding protein, located 90 bases from the araBAD and 60 bases from the araC transcriptional start points. A model for the mechanism of regulation of araBAD and araC expression by the catabolite gene-activator protein, P1, and P2 is proposed. An earlier model proposed by Ogden et al. (1980) is discussed.