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. 2014 Aug 1;5:390. doi: 10.3389/fmicb.2014.00390

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Copyright © 2014 Saier and Zhang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic diagram illustrating dual GlpR-mediated/cAMP-CRP-mediated control of (right) the level of glpFK transcription and (left) the rate of IS5 hopping into the activating site upstream of the glpFK promoter (directed mutation). With GlpR bound to its operators (O1–O4) (in the presence of GlpR and the absence of glycerol), transcription and IS5 hopping both occur at low rates. When GlpR is not bound to its operators (in the absence of GlpR or in the presence of glycerol), both transcriptional initiation and IS5 hopping increase about 10×. Binding of GlpR to operator O1 preferentially blocks IS5 insertion, while binding of GlpR to operator O4 preferentially blocks transcription as indicated. Binding of cAMP-CRP to its transcriptional activating sites, CrpI and CrpII, similarly inhibits IS5 hopping even though binding of this complex promotes glpFK transcription. Glucose inhibits IS5 insertion by a mechanism independent of glycerol, GlpR, cAMP, and CRP. (, activation; , inhibition or repression).

Inline graphic — Schematic diagram illustrating dual GlpR-mediated/cAMP-CRP-mediated control of (right) the level of glpFK transcription and (left) the rate of IS5 hopping into the activating site upstream of the glpFK promoter (directed mutation). With GlpR bound to its operators (O1–O4) (in the presence of GlpR and the absence of glycerol), transcription and IS5 hopping both occur at low rates. When GlpR is not bound to its operators (in the absence of GlpR or in the presence of glycerol), both transcriptional initiation and IS5 hopping increase about 10×. Binding of GlpR to operator O1 preferentially blocks IS5 insertion, while binding of GlpR to operator O4 preferentially blocks transcription as indicated. Binding of cAMP-CRP to its transcriptional activating sites, CrpI and CrpII, similarly inhibits IS5 hopping even though binding of this complex promotes glpFK transcription. Glucose inhibits IS5 insertion by a mechanism independent of glycerol, GlpR, cAMP, and CRP. (, activation; , inhibition or repression).