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The Association Between H3K4me3 and Antisense Transcription

Histone H3 lysine 4 trimethylation (H3K4me3) is well known to occur in the promoter region of genes for transcription activation. However, when investigating the H3K4me3 profiles in the mouse cerebrum and testis, we discovered that H3K4me3 also has a significant enrichment at the 3′ end of actively...

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Autores principales: Cui, Peng, Liu, Wanfei, Zhao, Yuhui, Lin, Qiang, Ding, Feng, Xin, Chengqi, Geng, Jianing, Song, Shuhui, Sun, Fanglin, Hu, Songnian, Yu, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5054153/
https://www.ncbi.nlm.nih.gov/pubmed/22768981
http://dx.doi.org/10.1016/j.gpb.2012.05.001
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author Cui, Peng
Liu, Wanfei
Zhao, Yuhui
Lin, Qiang
Ding, Feng
Xin, Chengqi
Geng, Jianing
Song, Shuhui
Sun, Fanglin
Hu, Songnian
Yu, Jun
author_facet Cui, Peng
Liu, Wanfei
Zhao, Yuhui
Lin, Qiang
Ding, Feng
Xin, Chengqi
Geng, Jianing
Song, Shuhui
Sun, Fanglin
Hu, Songnian
Yu, Jun
author_sort Cui, Peng
collection PubMed
description Histone H3 lysine 4 trimethylation (H3K4me3) is well known to occur in the promoter region of genes for transcription activation. However, when investigating the H3K4me3 profiles in the mouse cerebrum and testis, we discovered that H3K4me3 also has a significant enrichment at the 3′ end of actively transcribed (sense) genes, named as 3′-H3K4me3. 3′-H3K4me3 is associated with ∼15% of protein-coding genes in both tissues. In addition, we examined the transcriptional initiation signals including RNA polymerase II (RNAPII) binding sites and 5′-CAGE-tag that marks transcriptional start sites. Interestingly, we found that 3′-H3K4me3 is associated with the initiation of antisense transcription. Furthermore, 3′-H3K4me3 modification levels correlate positively with the antisense expression levels of the associated sense genes, implying that 3′-H3K4me3 is involved in the activation of antisense transcription. Taken together, our findings suggest that H3K4me3 may be involved in the regulation of antisense transcription that initiates from the 3′ end of sense genes. In addition, a positive correlation was also observed between the expression of antisense and the associated sense genes with 3′-H3K4me3 modification. More importantly, we observed the 3′-H3K4me3 enrichment among genes in human, fruitfly and Arabidopsis, and found that the sequences of 3′-H3K4me3-marked regions are highly conserved and essentially indistinguishable from known promoters in vertebrate. Therefore, we speculate that these 3′-H3K4me3-marked regions may serve as potential promoters for antisense transcription and 3′-H3K4me3 appear to be a universal epigenetic feature in eukaryotes. Our results provide a novel insight into the epigenetic roles of H3K4me3 and the regulatory mechanism of antisense transcription.
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spelling pubmed-50541532016-10-14 The Association Between H3K4me3 and Antisense Transcription Cui, Peng Liu, Wanfei Zhao, Yuhui Lin, Qiang Ding, Feng Xin, Chengqi Geng, Jianing Song, Shuhui Sun, Fanglin Hu, Songnian Yu, Jun Genomics Proteomics Bioinformatics Original Research Histone H3 lysine 4 trimethylation (H3K4me3) is well known to occur in the promoter region of genes for transcription activation. However, when investigating the H3K4me3 profiles in the mouse cerebrum and testis, we discovered that H3K4me3 also has a significant enrichment at the 3′ end of actively transcribed (sense) genes, named as 3′-H3K4me3. 3′-H3K4me3 is associated with ∼15% of protein-coding genes in both tissues. In addition, we examined the transcriptional initiation signals including RNA polymerase II (RNAPII) binding sites and 5′-CAGE-tag that marks transcriptional start sites. Interestingly, we found that 3′-H3K4me3 is associated with the initiation of antisense transcription. Furthermore, 3′-H3K4me3 modification levels correlate positively with the antisense expression levels of the associated sense genes, implying that 3′-H3K4me3 is involved in the activation of antisense transcription. Taken together, our findings suggest that H3K4me3 may be involved in the regulation of antisense transcription that initiates from the 3′ end of sense genes. In addition, a positive correlation was also observed between the expression of antisense and the associated sense genes with 3′-H3K4me3 modification. More importantly, we observed the 3′-H3K4me3 enrichment among genes in human, fruitfly and Arabidopsis, and found that the sequences of 3′-H3K4me3-marked regions are highly conserved and essentially indistinguishable from known promoters in vertebrate. Therefore, we speculate that these 3′-H3K4me3-marked regions may serve as potential promoters for antisense transcription and 3′-H3K4me3 appear to be a universal epigenetic feature in eukaryotes. Our results provide a novel insight into the epigenetic roles of H3K4me3 and the regulatory mechanism of antisense transcription. Elsevier 2012-04 2012-06-08 /pmc/articles/PMC5054153/ /pubmed/22768981 http://dx.doi.org/10.1016/j.gpb.2012.05.001 Text en © 2012 Beijing Institute of Genomics, Chinese Academy of Sciences and Genetics Society of China. Published by Elsevier Ltd and Science Press. All rights reserved. http://creativecommons.org/licenses/by-nc-sa/3.0/ This is an open access article under the CC BY-NC-SA license (http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Original Research
Cui, Peng
Liu, Wanfei
Zhao, Yuhui
Lin, Qiang
Ding, Feng
Xin, Chengqi
Geng, Jianing
Song, Shuhui
Sun, Fanglin
Hu, Songnian
Yu, Jun
The Association Between H3K4me3 and Antisense Transcription
title The Association Between H3K4me3 and Antisense Transcription
title_full The Association Between H3K4me3 and Antisense Transcription
title_fullStr The Association Between H3K4me3 and Antisense Transcription
title_full_unstemmed The Association Between H3K4me3 and Antisense Transcription
title_short The Association Between H3K4me3 and Antisense Transcription
title_sort association between h3k4me3 and antisense transcription
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5054153/
https://www.ncbi.nlm.nih.gov/pubmed/22768981
http://dx.doi.org/10.1016/j.gpb.2012.05.001
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