Functional analysis of the role of CggR (central glycolytic gene regulator) in Lactobacillus plantarum by transcriptome analysis
Article first published online: 29 OCT 2010
© 2010 The Authors. Journal compilation © 2010 Society for Applied Microbiology and Blackwell Publishing Ltd
Special Issue: Lactic Acid Bacteria. Editors: Michiel Kleerebezem and Willem M. de Vos.
Volume 4, Issue 3, pages 345–356, May 2011
How to Cite
Rud, I., Naterstad, K., Bongers, R. S., Molenaar, D., Kleerebezem, M. and Axelsson, L. (2011), Functional analysis of the role of CggR (central glycolytic gene regulator) in Lactobacillus plantarum by transcriptome analysis. Microbial Biotechnology, 4: 345–356. doi: 10.1111/j.1751-7915.2010.00223.x
- Issue published online: 25 APR 2011
- Article first published online: 29 OCT 2010
- Received 1 June, 2010; accepted 14 September, 2010.
The level of the central glycolytic gene regulator (CggR) was engineered in Lactobacillus plantarum NC8 and WCFS1 by overexpression and in-frame mutation of the cggR gene in order to evaluate its regulatory role on the glycolytic gap operon and the glycolytic flux. The repressor role of CggR on the gap operon was indicated through identification of a putative CggR operator and transcriptome analysis, which coincided with decreased growth rate and glycolytic flux when cggR was overexpressed in NC8 and WCFS1. The mutation of cggR did not affect regulation of the gap operon, indicating a more prominent regulatory role of CggR on the gap operon under other conditions than tested (e.g. fermentation of other sugars than glucose or ribose) and when the level of the putative effector molecule FBP is reduced. Interestingly, the mutation of cggR had several effects in NC8, i.e. increased growth rate and glycolytic flux and regulation of genes with functions associated with glycerol and pyruvate metabolism; however, no effects were observed in WCFS1. The affected genes in NC8 are presumably regulated by CcpA, since putative CRE sites were identified in their upstream regions. The interconnection with CggR and CcpA-mediated control on growth and metabolism needs to be further elucidated.