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Co-ordinated regulation of gluconate catabolism and glucose uptake in Corynebacterium glutamicum by two functionally equivalent transcriptional regulators, GntR1 and GntR2
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...
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Formato: | Texto |
Lenguaje: | English |
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Blackwell Publishing Ltd
2008
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2230225/ https://www.ncbi.nlm.nih.gov/pubmed/18047570 http://dx.doi.org/10.1111/j.1365-2958.2007.06020.x |
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author | Frunzke, Julia Engels, Verena Hasenbein, Sonja Gätgens, Cornelia Bott, Michael |
author_facet | Frunzke, Julia Engels, Verena Hasenbein, Sonja Gätgens, Cornelia Bott, Michael |
author_sort | Frunzke, Julia |
collection | PubMed |
description | 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 EII(Glc) 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. |
format | Text |
id | pubmed-2230225 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-22302252008-02-12 Co-ordinated regulation of gluconate catabolism and glucose uptake in Corynebacterium glutamicum by two functionally equivalent transcriptional regulators, GntR1 and GntR2 Frunzke, Julia Engels, Verena Hasenbein, Sonja Gätgens, Cornelia Bott, Michael Mol Microbiol Research Articles 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 EII(Glc) 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. Blackwell Publishing Ltd 2008-01 2007-11-06 /pmc/articles/PMC2230225/ /pubmed/18047570 http://dx.doi.org/10.1111/j.1365-2958.2007.06020.x Text en © 2007 The Authors Journal compilation © 2007 Blackwell Publishing Ltd https://creativecommons.org/licenses/by/2.5/ Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation. |
spellingShingle | Research Articles Frunzke, Julia Engels, Verena Hasenbein, Sonja Gätgens, Cornelia Bott, Michael Co-ordinated regulation of gluconate catabolism and glucose uptake in Corynebacterium glutamicum by two functionally equivalent transcriptional regulators, GntR1 and GntR2 |
title | Co-ordinated regulation of gluconate catabolism and glucose uptake in Corynebacterium glutamicum by two functionally equivalent transcriptional regulators, GntR1 and GntR2 |
title_full | Co-ordinated regulation of gluconate catabolism and glucose uptake in Corynebacterium glutamicum by two functionally equivalent transcriptional regulators, GntR1 and GntR2 |
title_fullStr | Co-ordinated regulation of gluconate catabolism and glucose uptake in Corynebacterium glutamicum by two functionally equivalent transcriptional regulators, GntR1 and GntR2 |
title_full_unstemmed | Co-ordinated regulation of gluconate catabolism and glucose uptake in Corynebacterium glutamicum by two functionally equivalent transcriptional regulators, GntR1 and GntR2 |
title_short | Co-ordinated regulation of gluconate catabolism and glucose uptake in Corynebacterium glutamicum by two functionally equivalent transcriptional regulators, GntR1 and GntR2 |
title_sort | co-ordinated regulation of gluconate catabolism and glucose uptake in corynebacterium glutamicum by two functionally equivalent transcriptional regulators, gntr1 and gntr2 |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2230225/ https://www.ncbi.nlm.nih.gov/pubmed/18047570 http://dx.doi.org/10.1111/j.1365-2958.2007.06020.x |
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