Substrate induction and catabolite repression of the Streptomyces coelicolor glycerol operon are mediated through the GylR protein

Abstract

The pathway for glycerol catabolism in Streptomyces coelicolor is determined by the gylCABX operon, which is transcribed from two closely spaced glycerol-inducible, glucose-repressible promoters. Glucose (or catabolite) repression of gyl is known to be exerted by a general catabolite repression system in which the soluble glucose kinase plays a central role. The gylR gene is contained in a separate glycerol-inducible, weakly glucose-repressible transcription unit immediately upstream from the gyl operon. The role of gylR in the regulation of gyl transcription was assessed by introducing specific null mutations into the chromosomal gylR gene. Direct quantification of gyl transcripts from the gylR null mutants grown on different carbon sources demonstrated that GylR is the repressor of the gylCABX operon and also revealed that GylR functions as a negative autoregulator. Moreover, the transcriptional analysis revealed that the gylR null mutants were relieved of glucose repression of both gylCABX and gylR. We conclude that both substrate induction and catabolite repression of gyl are mediated through the GylR protein. This is the first direct evidence that catabolite repression in Streptomyces is not exerted at the transcriptional level by a general 'catabolite repressor protein'. Models for catabolite repression are discussed.