DNase and restriction site protection studies show that cAMP and its receptor protein (CRP) bind to the promoter of the ilvB operon at approximately position -44 to -82. This region contains sequences that are homologous to those found in other CRP-dependent promoters. In vitro transcription from the ilvB promoter was markedly increased by the addition of cAMP and CRP. This stimulation was not found when the ilvB template lacked the proposed CRP binding site. cAMP-CRP did not alter the extent of transcription termination within the ilvB leader suggesting that this regulatory system may be independent of the attenuation mechanism involved in the negative control of this operon. The results of restriction enzyme site protection studies and experiments with altered promoter fragments indicate that the mechanism for CRP stimulation of the ilvB operon may be similar to a model recently proposed for lac (1).
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