Catabolite repression of inositol dehydrogenase and gluconate kinase syntheses in Bacillus subtilis

Abstract

The regulation of induction of inositol dehydrogenase (EC 1.1.1.18) and gluconate kinase (EC 2.7.1.12) was studied in Bacillus subtilis. Inositol dehydrogenase is induced by myo-inositol and gluconate kinase is induced by D-gluconate. Both inductions were strongly repressed by rapidly metabolizable carbohydrates such as D-glucose, D-mannose, D-fructose and glycerol (D-glucose had the strongest repressive effect) but they were weakly repressed by slowly metabolizable carbohydrates. Although each carbohydrate exerted a stronger effect on the induction of inositol dehydrogenase than that of gluconate kinase, it showed a similar tendency with respect to the degree of repression of each induction. This catabolite repression could not be diminished by addition of cyclic AMP to medium. In addition, non-metabolizable D-glucose analogues had no or weak repressive effects. On the assumption that rapidly metabolizable carbohydrates might be metabolized to repress both inductions, it was investigated whether several mutants blocked in the Embden-Meyerhof pathway could produce metabolite(s) (repressor) to repress them. A phosphoglycerate kinase (EC 2.7.2.3) deficient mutant could produce the repressor from D-glucose, D-mannose, D-fructose and glycerol but other mutants could not produce it from carbohydrates unable to be metabolized in each mutant. Thus, catabolite repression of both enzyme inductions seemed to be under similar regulation. The identification of the possible repressor of the induction of in of inositol dehydrogenase and gluconate kinase in vivo was discussed.

Catabolite repression of the Bacillus subtilis gnt operon exerted by two catabolite‐responsive elements

“…The specific activities were corrected for the CAT activity present in the cells of the corresponding strain bearing vector pPL603B Each value is the average of three to five determinations of the gnt operon gntR (credown), although CcpA itself binds to DNA only non-specifically . Based on these findings, as well as those reported previously (Nihashi and Fujita, 1984;Deutscher eta/., 1995), we proposed a molecular mechanism for the catabolite repression in B. subtilis involving CcpA, P-ser-HPr and cre . We report in this paper that, in addition to credown, the gnt operon contains another cre located in the promoter region (meup), which is also responsible for CcpA-dependent catabolite repression of the gnt operon.…”

How Phosphotransferase System-Related Protein Phosphorylation Regulates Carbohydrate Metabolism in Bacteria

“…A connection between the phosphorylation of HPr at Ser-46 and CCR was suggested by the observation that CCR in B. subtilis requires the metabolism of the repressing sugar (490,606). In gram-negative bacteria, the transport of a carbohydrate via the PTS is sufficient to elicit CCR.…”

Carbon Catabolite Control of the Metabolic Network inBacillus subtilis

“…[68][69][70] Mutants unable to produce FBP do not exhibit CCR of myo-inositol dehydrogenase, acetoin dehydrogenase, or gluconate kinase, implying the presence of a common regulatory mechanism underlying CCR in B. subtilis. The role of FBP is to stimulate phosphorylation of HPr at Ser-46, which is catalyzed by HPr kinase/phosphatase (HPrK/ P), as was verified later.…”