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The preservation of bidirectional promoter architecture in eukaryotes: what is the driving force?
BACKGROUND: The bidirectional gene architecture has been studied in many organisms, and the conservation of bidirectional arrangement has received considerable attention. However, the explanation for the evolutionary conservation about this genomic structure is still insufficient. In this study the...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403606/ https://www.ncbi.nlm.nih.gov/pubmed/23046569 http://dx.doi.org/10.1186/1752-0509-6-S1-S21 |
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author | Xu, Chao Chen, Jiajia Shen, Bairong |
author_facet | Xu, Chao Chen, Jiajia Shen, Bairong |
author_sort | Xu, Chao |
collection | PubMed |
description | BACKGROUND: The bidirectional gene architecture has been studied in many organisms, and the conservation of bidirectional arrangement has received considerable attention. However, the explanation for the evolutionary conservation about this genomic structure is still insufficient. In this study the large scale identification and pathway enrichment analysis for bidirectional genes were performed in several eukaryotes and the comparative analysis of this arrangement between human and mouse were dissected for the purpose of discovering the driving force of the preservation of this genomic structure. RESULTS: We identified the bidirectional gene pairs in eight different species and found this structure to be prevalent in eukaryotes. The pathway enrichment analysis indicated the bidirectional genes at the genome level are conserved in certain pathways, such as the DNA repair and some other fundamental cellular pathways. The comparative analysis about the gene expression, function, between human and mouse bidirectional genes were also performed and we observed that the selective force of this architecture doesn't derive from the co-regulation between paired genes, but the functional bias of bidirectional genes at whole genome level is observed strengthened during evolution. CONCLUSIONS: Our result validated the coexpression of bidirectional genes; however failed to support their functional relevance. The conservation of bidirectional promoters seems not the result of functional connection between paired genes, but the functional bias at whole genome level, which imply that the genome-wide functional constraint is important for the conservation of bidirectional structure. |
format | Online Article Text |
id | pubmed-3403606 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-34036062012-07-27 The preservation of bidirectional promoter architecture in eukaryotes: what is the driving force? Xu, Chao Chen, Jiajia Shen, Bairong BMC Syst Biol Research BACKGROUND: The bidirectional gene architecture has been studied in many organisms, and the conservation of bidirectional arrangement has received considerable attention. However, the explanation for the evolutionary conservation about this genomic structure is still insufficient. In this study the large scale identification and pathway enrichment analysis for bidirectional genes were performed in several eukaryotes and the comparative analysis of this arrangement between human and mouse were dissected for the purpose of discovering the driving force of the preservation of this genomic structure. RESULTS: We identified the bidirectional gene pairs in eight different species and found this structure to be prevalent in eukaryotes. The pathway enrichment analysis indicated the bidirectional genes at the genome level are conserved in certain pathways, such as the DNA repair and some other fundamental cellular pathways. The comparative analysis about the gene expression, function, between human and mouse bidirectional genes were also performed and we observed that the selective force of this architecture doesn't derive from the co-regulation between paired genes, but the functional bias of bidirectional genes at whole genome level is observed strengthened during evolution. CONCLUSIONS: Our result validated the coexpression of bidirectional genes; however failed to support their functional relevance. The conservation of bidirectional promoters seems not the result of functional connection between paired genes, but the functional bias at whole genome level, which imply that the genome-wide functional constraint is important for the conservation of bidirectional structure. BioMed Central 2012-07-16 /pmc/articles/PMC3403606/ /pubmed/23046569 http://dx.doi.org/10.1186/1752-0509-6-S1-S21 Text en Copyright ©2012 Xu 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 Xu, Chao Chen, Jiajia Shen, Bairong The preservation of bidirectional promoter architecture in eukaryotes: what is the driving force? |
title | The preservation of bidirectional promoter architecture in eukaryotes: what is the driving force? |
title_full | The preservation of bidirectional promoter architecture in eukaryotes: what is the driving force? |
title_fullStr | The preservation of bidirectional promoter architecture in eukaryotes: what is the driving force? |
title_full_unstemmed | The preservation of bidirectional promoter architecture in eukaryotes: what is the driving force? |
title_short | The preservation of bidirectional promoter architecture in eukaryotes: what is the driving force? |
title_sort | preservation of bidirectional promoter architecture in eukaryotes: what is the driving force? |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403606/ https://www.ncbi.nlm.nih.gov/pubmed/23046569 http://dx.doi.org/10.1186/1752-0509-6-S1-S21 |
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