Cellobiose-Mediated Gene Expression in Streptococcus pneumoniae: A Repressor Function of the Novel GntR-Type Regulator BguR

The human pathogen Streptococcus pneumoniae has the ability to use the carbon- and energy source cellobiose due to the presence of a cellobiose-utilizing gene cluster (cel locus) in its genome. This system is regulated by the cellobiose-dependent transcriptional activator CelR, which has been previo...

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Main Authors: Shafeeq, Sulman, Kuipers, Oscar P., Kloosterman, Tomas G.
Format: Online
Language:English
Published: Public Library of Science 2013
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3585215/
id pubmed-3585215
recordtype oai_dc
spelling pubmed-35852152013-03-06 Cellobiose-Mediated Gene Expression in Streptococcus pneumoniae: A Repressor Function of the Novel GntR-Type Regulator BguR Shafeeq, Sulman Kuipers, Oscar P. Kloosterman, Tomas G. Research Article The human pathogen Streptococcus pneumoniae has the ability to use the carbon- and energy source cellobiose due to the presence of a cellobiose-utilizing gene cluster (cel locus) in its genome. This system is regulated by the cellobiose-dependent transcriptional activator CelR, which has been previously shown to contribute to pneumococcal virulence. To get a broader understanding of the response of S. pneumoniae to cellobiose, we compared the pneumococcal transcriptome during growth on glucose as the main carbon source to that with cellobiose as the main carbon source. The expression of various carbon metabolic genes was altered, including a PTS operon (which we here denote as the bgu operon) that has high similarity with the cel locus. In contrast to the cel locus, the bgu operon is conserved in all sequenced strains of S. pneumoniae, indicating an important physiological function in the lifestyle of pneumococci. We next characterized the transcriptional regulation of the bgu operon in more detail. Its expression was increased in the presence of cellobiose, and decreased in the presence of glucose. A novel GntR-type transcriptional regulator (which we here denote as BguR) was shown to act as a transcriptional repressor of the bgu operon and its repressive effect was relieved in the presence of cellobiose. BguR-dependent repression was demonstrated to be mediated by a 20-bp DNA operator site (5′-AAAAATGTCTAGACAAATTT-3′) present in PbguA, as verified by promoter truncation experiments. In conclusion, we have identified a new cellobiose-responsive PTS operon, together with its transcriptional regulator in S. pneumoniae. Public Library of Science 2013-02-28 /pmc/articles/PMC3585215/ /pubmed/23469031 http://dx.doi.org/10.1371/journal.pone.0057586 Text en © 2013 Shafeeq et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Shafeeq, Sulman
Kuipers, Oscar P.
Kloosterman, Tomas G.
spellingShingle Shafeeq, Sulman
Kuipers, Oscar P.
Kloosterman, Tomas G.
Cellobiose-Mediated Gene Expression in Streptococcus pneumoniae: A Repressor Function of the Novel GntR-Type Regulator BguR
author_facet Shafeeq, Sulman
Kuipers, Oscar P.
Kloosterman, Tomas G.
author_sort Shafeeq, Sulman
title Cellobiose-Mediated Gene Expression in Streptococcus pneumoniae: A Repressor Function of the Novel GntR-Type Regulator BguR
title_short Cellobiose-Mediated Gene Expression in Streptococcus pneumoniae: A Repressor Function of the Novel GntR-Type Regulator BguR
title_full Cellobiose-Mediated Gene Expression in Streptococcus pneumoniae: A Repressor Function of the Novel GntR-Type Regulator BguR
title_fullStr Cellobiose-Mediated Gene Expression in Streptococcus pneumoniae: A Repressor Function of the Novel GntR-Type Regulator BguR
title_full_unstemmed Cellobiose-Mediated Gene Expression in Streptococcus pneumoniae: A Repressor Function of the Novel GntR-Type Regulator BguR
title_sort cellobiose-mediated gene expression in streptococcus pneumoniae: a repressor function of the novel gntr-type regulator bgur
description The human pathogen Streptococcus pneumoniae has the ability to use the carbon- and energy source cellobiose due to the presence of a cellobiose-utilizing gene cluster (cel locus) in its genome. This system is regulated by the cellobiose-dependent transcriptional activator CelR, which has been previously shown to contribute to pneumococcal virulence. To get a broader understanding of the response of S. pneumoniae to cellobiose, we compared the pneumococcal transcriptome during growth on glucose as the main carbon source to that with cellobiose as the main carbon source. The expression of various carbon metabolic genes was altered, including a PTS operon (which we here denote as the bgu operon) that has high similarity with the cel locus. In contrast to the cel locus, the bgu operon is conserved in all sequenced strains of S. pneumoniae, indicating an important physiological function in the lifestyle of pneumococci. We next characterized the transcriptional regulation of the bgu operon in more detail. Its expression was increased in the presence of cellobiose, and decreased in the presence of glucose. A novel GntR-type transcriptional regulator (which we here denote as BguR) was shown to act as a transcriptional repressor of the bgu operon and its repressive effect was relieved in the presence of cellobiose. BguR-dependent repression was demonstrated to be mediated by a 20-bp DNA operator site (5′-AAAAATGTCTAGACAAATTT-3′) present in PbguA, as verified by promoter truncation experiments. In conclusion, we have identified a new cellobiose-responsive PTS operon, together with its transcriptional regulator in S. pneumoniae.
publisher Public Library of Science
publishDate 2013
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3585215/
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