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Transcriptional analysis of the recA gene of Streptococcus thermophilus

BACKGROUND: RecA is a highly conserved prokaryotic protein that not only plays several important roles connected to DNA metabolism but also affects the cell response to various stress conditions. While RecA is highly conserved, the mechanism of transcriptional regulation of its structural gene is le...

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Autores principales: Giliberti, Gabriele, Baccigalupi, Loredana, Cordone, Angelina, Ricca, Ezio, De Felice, Maurilio
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1592510/
https://www.ncbi.nlm.nih.gov/pubmed/16972988
http://dx.doi.org/10.1186/1475-2859-5-29
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author Giliberti, Gabriele
Baccigalupi, Loredana
Cordone, Angelina
Ricca, Ezio
De Felice, Maurilio
author_facet Giliberti, Gabriele
Baccigalupi, Loredana
Cordone, Angelina
Ricca, Ezio
De Felice, Maurilio
author_sort Giliberti, Gabriele
collection PubMed
description BACKGROUND: RecA is a highly conserved prokaryotic protein that not only plays several important roles connected to DNA metabolism but also affects the cell response to various stress conditions. While RecA is highly conserved, the mechanism of transcriptional regulation of its structural gene is less conserved. In Escherichia coli the LexA protein acts as a recA repressor and is able, in response to DNA damage, of RecA-promoted self-cleavage, thus allowing recA transcription. The LexA paradigm, although confirmed in a wide number of cases, is not universally valid. In some cases LexA does not control recA transcription while in other RecA-containing bacteria a LexA homologue is not present. RESULTS: We have studied the recA transcriptional regulation in S. thermophilus, a bacterium that does not contain a LexA homologue. We have characterized the promoter region of the gene and observed that its expression is strongly induced by DNA damage. The analysis of deletion mutants and of translational gene fusions showed that a DNA region of 83 base pairs, containg the recA promoter and the transcriptional start site, is sufficient to ensure normal expression of the gene. Unlike LexA of E. coli, the factor controlling recA expression in S. thermophilus acts in a RecA-independent way since recA induction was observed in a strain carrying a recA null mutation. CONCLUSION: In S. thermophilus, as in many other bacteria,recA expression is strongly induced by DNA damage, however, in this organism expression of the gene is controlled by a factor different from those well characterized in other bacteria. A small DNA region extending from 62 base pairs upstream of the recA transcriptional start site to 21 base pairs downstream of it carries all the information needed for normal regulation of the S. thermophilus recA gene.
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spelling pubmed-15925102006-10-07 Transcriptional analysis of the recA gene of Streptococcus thermophilus Giliberti, Gabriele Baccigalupi, Loredana Cordone, Angelina Ricca, Ezio De Felice, Maurilio Microb Cell Fact Research BACKGROUND: RecA is a highly conserved prokaryotic protein that not only plays several important roles connected to DNA metabolism but also affects the cell response to various stress conditions. While RecA is highly conserved, the mechanism of transcriptional regulation of its structural gene is less conserved. In Escherichia coli the LexA protein acts as a recA repressor and is able, in response to DNA damage, of RecA-promoted self-cleavage, thus allowing recA transcription. The LexA paradigm, although confirmed in a wide number of cases, is not universally valid. In some cases LexA does not control recA transcription while in other RecA-containing bacteria a LexA homologue is not present. RESULTS: We have studied the recA transcriptional regulation in S. thermophilus, a bacterium that does not contain a LexA homologue. We have characterized the promoter region of the gene and observed that its expression is strongly induced by DNA damage. The analysis of deletion mutants and of translational gene fusions showed that a DNA region of 83 base pairs, containg the recA promoter and the transcriptional start site, is sufficient to ensure normal expression of the gene. Unlike LexA of E. coli, the factor controlling recA expression in S. thermophilus acts in a RecA-independent way since recA induction was observed in a strain carrying a recA null mutation. CONCLUSION: In S. thermophilus, as in many other bacteria,recA expression is strongly induced by DNA damage, however, in this organism expression of the gene is controlled by a factor different from those well characterized in other bacteria. A small DNA region extending from 62 base pairs upstream of the recA transcriptional start site to 21 base pairs downstream of it carries all the information needed for normal regulation of the S. thermophilus recA gene. BioMed Central 2006-09-14 /pmc/articles/PMC1592510/ /pubmed/16972988 http://dx.doi.org/10.1186/1475-2859-5-29 Text en Copyright © 2006 Giliberti et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Giliberti, Gabriele
Baccigalupi, Loredana
Cordone, Angelina
Ricca, Ezio
De Felice, Maurilio
Transcriptional analysis of the recA gene of Streptococcus thermophilus
title Transcriptional analysis of the recA gene of Streptococcus thermophilus
title_full Transcriptional analysis of the recA gene of Streptococcus thermophilus
title_fullStr Transcriptional analysis of the recA gene of Streptococcus thermophilus
title_full_unstemmed Transcriptional analysis of the recA gene of Streptococcus thermophilus
title_short Transcriptional analysis of the recA gene of Streptococcus thermophilus
title_sort transcriptional analysis of the reca gene of streptococcus thermophilus
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1592510/
https://www.ncbi.nlm.nih.gov/pubmed/16972988
http://dx.doi.org/10.1186/1475-2859-5-29
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