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CGGBP1 mitigates cytosine methylation at repetitive DNA sequences
BACKGROUND: CGGBP1 is a repetitive DNA-binding transcription regulator with target sites at CpG-rich sequences such as CGG repeats and Alu-SINEs and L1-LINEs. The role of CGGBP1 as a possible mediator of CpG methylation however remains unknown. At CpG-rich sequences cytosine methylation is a major m...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4432828/ https://www.ncbi.nlm.nih.gov/pubmed/25981527 http://dx.doi.org/10.1186/s12864-015-1593-2 |
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author | Agarwal, Prasoon Collier, Paul Fritz, Markus Hsi-Yang Benes, Vladimir Wiklund, Helena Jernberg Westermark, Bengt Singh, Umashankar |
author_facet | Agarwal, Prasoon Collier, Paul Fritz, Markus Hsi-Yang Benes, Vladimir Wiklund, Helena Jernberg Westermark, Bengt Singh, Umashankar |
author_sort | Agarwal, Prasoon |
collection | PubMed |
description | BACKGROUND: CGGBP1 is a repetitive DNA-binding transcription regulator with target sites at CpG-rich sequences such as CGG repeats and Alu-SINEs and L1-LINEs. The role of CGGBP1 as a possible mediator of CpG methylation however remains unknown. At CpG-rich sequences cytosine methylation is a major mechanism of transcriptional repression. Concordantly, gene-rich regions typically carry lower levels of CpG methylation than the repetitive elements. It is well known that at interspersed repeats Alu-SINEs and L1-LINEs high levels of CpG methylation constitute a transcriptional silencing and retrotransposon inactivating mechanism. RESULTS: Here, we have studied genome-wide CpG methylation with or without CGGBP1-depletion. By high throughput sequencing of bisulfite-treated genomic DNA we have identified CGGBP1 to be a negative regulator of CpG methylation at repetitive DNA sequences. In addition, we have studied CpG methylation alterations on Alu and L1 retrotransposons in CGGBP1-depleted cells using a novel bisulfite-treatment and high throughput sequencing approach. CONCLUSIONS: The results clearly show that CGGBP1 is a possible bidirectional regulator of CpG methylation at Alus, and acts as a repressor of methylation at L1 retrotransposons. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12864-015-1593-2) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4432828 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-44328282015-05-16 CGGBP1 mitigates cytosine methylation at repetitive DNA sequences Agarwal, Prasoon Collier, Paul Fritz, Markus Hsi-Yang Benes, Vladimir Wiklund, Helena Jernberg Westermark, Bengt Singh, Umashankar BMC Genomics Research Article BACKGROUND: CGGBP1 is a repetitive DNA-binding transcription regulator with target sites at CpG-rich sequences such as CGG repeats and Alu-SINEs and L1-LINEs. The role of CGGBP1 as a possible mediator of CpG methylation however remains unknown. At CpG-rich sequences cytosine methylation is a major mechanism of transcriptional repression. Concordantly, gene-rich regions typically carry lower levels of CpG methylation than the repetitive elements. It is well known that at interspersed repeats Alu-SINEs and L1-LINEs high levels of CpG methylation constitute a transcriptional silencing and retrotransposon inactivating mechanism. RESULTS: Here, we have studied genome-wide CpG methylation with or without CGGBP1-depletion. By high throughput sequencing of bisulfite-treated genomic DNA we have identified CGGBP1 to be a negative regulator of CpG methylation at repetitive DNA sequences. In addition, we have studied CpG methylation alterations on Alu and L1 retrotransposons in CGGBP1-depleted cells using a novel bisulfite-treatment and high throughput sequencing approach. CONCLUSIONS: The results clearly show that CGGBP1 is a possible bidirectional regulator of CpG methylation at Alus, and acts as a repressor of methylation at L1 retrotransposons. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12864-015-1593-2) contains supplementary material, which is available to authorized users. BioMed Central 2015-05-16 /pmc/articles/PMC4432828/ /pubmed/25981527 http://dx.doi.org/10.1186/s12864-015-1593-2 Text en © Agarwal et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Agarwal, Prasoon Collier, Paul Fritz, Markus Hsi-Yang Benes, Vladimir Wiklund, Helena Jernberg Westermark, Bengt Singh, Umashankar CGGBP1 mitigates cytosine methylation at repetitive DNA sequences |
title | CGGBP1 mitigates cytosine methylation at repetitive DNA sequences |
title_full | CGGBP1 mitigates cytosine methylation at repetitive DNA sequences |
title_fullStr | CGGBP1 mitigates cytosine methylation at repetitive DNA sequences |
title_full_unstemmed | CGGBP1 mitigates cytosine methylation at repetitive DNA sequences |
title_short | CGGBP1 mitigates cytosine methylation at repetitive DNA sequences |
title_sort | cggbp1 mitigates cytosine methylation at repetitive dna sequences |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4432828/ https://www.ncbi.nlm.nih.gov/pubmed/25981527 http://dx.doi.org/10.1186/s12864-015-1593-2 |
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