Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P51532 (transcriptional activator)
 6,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Bacillus subtilis gltAB genes, coding for the two subunits of glutamate synthase, are transcribed divergently from the gltC gene, encoding a LysR-type transcriptional activator of gltAB. The predicted gltA and gltC transcription start sites are separated by 51 to 52 bp. A 15-bp, consensus binding site (Box I) for LysR-type proteins was found centered at position -64 with respect to the gltA transcription start. This site was shown by mutational analysis to be required both for GltC-mediated activation of gltA and for autorepression of gltC. Box II, which is similar to Box I, is centered 22 bp downstream of Box I and overlaps the -35 region of the gltA promoter. Box II was found to be essential for activation of gltA but not for gltC autoregulation. Introduction of approximately one additional helical turn of DNA between Box I and Box II enhanced gltA expression 7- to 40-fold under nonactivating conditions and about 2-fold under activating conditions. Expression of gltA was dramatically decreased when the distance between Box I and Box II was altered by a nonintegral number of helical turns of DNA. gltC autorepression was abolished by most of the inserts between Box I and Box II but was augmented by adding one helical turn.
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PMID:Sites required for GltC-dependent regulation of Bacillus subtilis glutamate synthase expression. 755 59

Glutamate synthesis is the link between carbon and nitrogen metabolism. In Bacillus subtilis, glutamate is exclusively synthesized by the glutamate synthase encoded by the gltAB operon. The glutamate dehydrogenase RocG from B. subtilis is exclusively devoted to glutamate degradation rather than to its synthesis. The expression of the gltAB operon is induced by glucose and ammonium and strongly repressed by arginine. Regulation by glucose and arginine depends on the transcriptional activator protein GltC. The gltAB operon is constitutively expressed in a rocG mutant strain, but the molecular mechanism of negative control of gltAB expression by RocG has so far remained unknown. We studied the role of RocG in the intracellular accumulation of GltC. Furthermore, we considered the possibility that RocG might act as a transcription factor and be able to inhibit the expression of gltAB either by binding to the mRNA or to the promoter region of the gltAB operon. Finally, we asked whether a direct binding of RocG to GltC could be responsible for the inhibition of GltC. The genetic and biochemical data presented here show that the glutamate dehydrogenase RocG is able to bind to and concomitantly inactivate the activator protein GltC. This regulatory mechanism by the bifunctional enzyme RocG allows the tight control of glutamate metabolism by the availability of carbon and nitrogen sources.
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PMID:A regulatory protein-protein interaction governs glutamate biosynthesis in Bacillus subtilis: the glutamate dehydrogenase RocG moonlights in controlling the transcription factor GltC. 1760 97