REGULATION OF THE CARBOHYDRATE-METABOLISM IN LACTOCOCCUS-LACTIS AND OTHER LACTIC-ACID BACTERIA

Citation
Ej. Luesink et al., REGULATION OF THE CARBOHYDRATE-METABOLISM IN LACTOCOCCUS-LACTIS AND OTHER LACTIC-ACID BACTERIA, Le Lait, 78(1), 1998, pp. 69-76
Citations number
23
Categorie Soggetti
Food Science & Tenology
Journal title
ISSN journal
00237302
Volume
78
Issue
1
Year of publication
1998
Pages
69 - 76
Database
ISI
SICI code
0023-7302(1998)78:1<69:ROTCIL>2.0.ZU;2-C
Abstract
In recent years significant progress has been made in elucidating the regulation of carbohydrate metabolism in Lactococcus lactis and other lactic acid bacteria. Since insight in these mechanisms could provide valuable tools for metabolic engineering, an overview of the various g lobal control systems in Gram-positive bacteria is presented with spec ific attention for inducer exclusion, inducer expulsion and catabolite repression. Inducer exclusion is the phenomenon where the addition of a rapidly metabolizable sugar like glucose to the medium results in a reduced uptake of other sugars. Under the same circumstances another system called inducer expulsion is active that reduces the intracellul ar concentration of sugar phosphates by dephosphorylating sugar phosph ates and removing the sugars from the cell. Both mechanisms have been shown to depend on the phosphorylation state of residue serine 46 of t he phosphocarrier HPr by a metabolite-activated kinase. Apart from all osteric control, the carbohydrate metabolism can also be regulated at the transcriptional level. An example of transcriptional regulation is catabolite repression where the presence of a rapidly metabolizable s ugar in the medium reduces the transcription of genes required for the utilization of other sugars. Gram-positive bacteria mediate catabolit e repression via a transcriptional regulator, CcpA. To analyze the rol e of HPr and CcpA in the sugar metabolism in Lactococcus lactis, the g enes encoding HPr and CcpA, ptsH and ccpA respectively, have been clon ed and analyzed. (C) Inra/Elsevier, Paris.