Present address: Zentrum für Medizinische Biotechnologie, Universität Duisburg-Essen, D-45117 Essen, Germany.
Co-ordinated regulation of gluconate catabolism and glucose uptake in Corynebacterium glutamicum by two functionally equivalent transcriptional regulators, GntR1 and GntR2
Article first published online: 30 NOV 2007
Volume 67, Issue 2, pages 305–322, January 2008
How to Cite
Frunzke, J., Engels, V., Hasenbein, S., Gätgens, C. and Bott, M. (2008), Co-ordinated regulation of gluconate catabolism and glucose uptake in Corynebacterium glutamicum by two functionally equivalent transcriptional regulators, GntR1 and GntR2. Molecular Microbiology, 67: 305–322. doi: 10.1111/j.1365-2958.2007.06020.x
Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.
- Issue published online: 7 DEC 2007
- Article first published online: 30 NOV 2007
- Accepted 21 October, 2007.
Corynebacterium glutamicum is a Gram-positive soil bacterium that prefers the simultaneous catabolism of different carbon sources rather than their sequential utilization. This type of metabolism requires an adaptation of the utilization rates to the overall metabolic capacity. Here we show how two functionally redundant GntR-type transcriptional regulators, designated GntR1 and GntR2, co-ordinately regulate gluconate catabolism and glucose uptake. GntR1 and GntR2 strongly repress the genes encoding gluconate permease (gntP), gluconate kinase (gntK), and 6-phosphogluconate dehydrogenase (gnd) and weakly the pentose phosphate pathway genes organized in the tkt-tal-zwf-opcA-devB cluster. In contrast, ptsG encoding the EIIGlc permease of the glucose phosphotransferase system (PTS) is activated by GntR1 and GntR2. Gluconate and glucono-δ-lactone interfere with binding of GntR1 and GntR2 to their target promoters, leading to a derepression of the genes involved in gluconate catabolism and reduced ptsG expression. To our knowledge, this is the first example for gluconate-dependent transcriptional control of PTS genes. A mutant lacking both gntR1 and gntR2 shows a 60% lower glucose uptake rate and growth rate than the wild type when cultivated on glucose as sole carbon source. This growth defect can be complemented by plasmid-encoded GntR1 or GntR2.