Abstract
Transcription of ptsG encoding glucose-specific permease, enzyme IICB(Glc), in Escherichia coli is initiated from two promoters, P1 and P2. ptsG transcription is repressed by Mlc, a glucose-inducible regulator of carbohydrate metabolism. The regulation of ptsG P1 transcription is also under positive control by cyclic AMP receptor protein and cyclic AMP complex (CRP.cAMP) as observed in other Mlc regulon. We report here that Fis, one of the nucleoid-associated proteins, plays a key role in glucose induction of Mlc regulon. ptsG transcription was induced when wild-type cells were grown in the presence of glucose. However, in a fis mutant, the basal level of ptsG transcription was higher but decreased when cells were grown in the presence of glucose, which implies the possibility of regulatory interactions among Fis, Mlc, and CRP.cAMP. Footprinting experiments with various probes and transcription assays revealed that Fis assists both Mlc repression and CRP.cAMP activation of ptsG P1 through the formation of Fis.CRP.Mlc or Fis.CRP nucleoprotein complexes at ptsG P1 promoter depending on the availability of glucose in the growth medium. ptsG P2 transcription was inhibited by Fis and Mlc. Tighter Mlc repression and enhanced CRP.cAMP activation of ptsG P1 by Fis enable cells to regulate Mlc regulon efficiently by selectively controlling the concentration of enzyme IICB(Glc) that modulates Mlc activity.
Highlights
Transcription of ptsG encoding glucose-specific permease, enzyme IICBGlc, in Escherichia coli is initiated from two promoters, P1 and P2. ptsG transcription is repressed by Mlc, a glucose-inducible regulator of carbohydrate metabolism
Footprinting experiments with various probes and transcription assays revealed that Fis assists both Mlc repression and CRP1⁄7cAMP activation of ptsG P1 through the formation of Fis1⁄7CRP1⁄7Mlc or Fis1⁄7CRP nucleoprotein complexes at ptsG P1 promoter depending on the availability of glucose in the growth medium. ptsG P2 transcription was inhibited by Fis and Mlc
These results suggest that Fis is required for both the repression of ptsG P1 by Mlc and the activation of ptsG P1 under limited concentration of CRP1⁄7cAMP [6, 7]
Summary
FORMATION OF EITHER ACTIVATING OR REPRESSING NUCLEOPROTEIN COMPLEX IN RESPONSE TO GLUCOSE*. Footprinting experiments with various probes and transcription assays revealed that Fis assists both Mlc repression and CRP1⁄7cAMP activation of ptsG P1 through the formation of Fis1⁄7CRP1⁄7Mlc or Fis1⁄7CRP nucleoprotein complexes at ptsG P1 promoter depending on the availability of glucose in the growth medium. PtsG P2 transcription was inhibited by Fis and Mlc. Tighter Mlc repression and enhanced CRP1⁄7cAMP activation of ptsG P1 by Fis enable cells to regulate Mlc regulon efficiently by selectively controlling the concentration of enzyme IICBGlc that modulates Mlc activity. In addition to the regulations at the transcriptional level, expression of ptsG is regulated post-transcriptionally via modulation of ptsG mRNA stability in response to glycolytic flux in the cells [17] These observations suggest that the expression of ptsG is regulated in a highly complex and dynamic manner in response to various growth environments, as well as to the availability of glucose. We report here that E. coli can regulate the expression of ptsG prior to the modulation of other Mlc regulon because of the selective enhancement of Mlc-dependent repression, as well as CRP-dependent activation of ptsG in the presence of Fis
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