Transcriptome and H3K27 tri-methylation profiling of Ezh2-deficient lung epithelium
The adaptation of the lungs to air breathing at birth requires the fine orchestration of different processes to control lung morphogenesis and progenitor cell differentiation. However, there is little understanding of the role that epigenetic modifiers play in the control of lung development. We fou...
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Format: | Article |
Language: | English |
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Elsevier
2015-09-01
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Series: | Genomics Data |
Online Access: | http://www.sciencedirect.com/science/article/pii/S2213596015001506 |
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author | Aliaksei Z. Holik Laura A. Galvis Aaron T.L. Lun Matthew E. Ritchie Marie-Liesse Asselin-Labat |
author_facet | Aliaksei Z. Holik Laura A. Galvis Aaron T.L. Lun Matthew E. Ritchie Marie-Liesse Asselin-Labat |
author_sort | Aliaksei Z. Holik |
collection | DOAJ |
description | The adaptation of the lungs to air breathing at birth requires the fine orchestration of different processes to control lung morphogenesis and progenitor cell differentiation. However, there is little understanding of the role that epigenetic modifiers play in the control of lung development. We found that the histone methyl transferase Ezh2 plays a critical role in lung lineage specification and survival at birth. We performed a genome-wide transcriptome study combined with a genome-wide analysis of the distribution of H3K27 tri-methylation marks to interrogate the role of Ezh2 in lung epithelial cells. Lung cells isolated from Ezh2-deficient and control mice at embryonic day E16.5 were sorted into epithelial and mesenchymal populations based on EpCAM expression. This enabled us to dissect the transcriptional and epigenetic changes induced by the loss of Ezh2 specifically in the lung epithelium. Here we provide a detailed description of the analysis of the RNA-seq and ChIP-seq data, including quality control, read mapping, differential expression and differential binding analyses, as well as visualisation methods used to present the data. These data can be accessed from the Gene Expression Omnibus database (super-series accession number GSE57393). |
first_indexed | 2024-12-13T10:26:28Z |
format | Article |
id | doaj.art-0be334ea2abb491baee2f4963d6b4067 |
institution | Directory Open Access Journal |
issn | 2213-5960 |
language | English |
last_indexed | 2024-12-13T10:26:28Z |
publishDate | 2015-09-01 |
publisher | Elsevier |
record_format | Article |
series | Genomics Data |
spelling | doaj.art-0be334ea2abb491baee2f4963d6b40672022-12-21T23:51:02ZengElsevierGenomics Data2213-59602015-09-015C34635110.1016/j.gdata.2015.07.006Transcriptome and H3K27 tri-methylation profiling of Ezh2-deficient lung epitheliumAliaksei Z. Holik0Laura A. Galvis1Aaron T.L. Lun2Matthew E. Ritchie3Marie-Liesse Asselin-Labat4ACRF Stem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, AustraliaACRF Stem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, AustraliaDepartment of Medical Biology, The University of Melbourne, Parkville, Victoria 3010, AustraliaDepartment of Medical Biology, The University of Melbourne, Parkville, Victoria 3010, AustraliaACRF Stem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, AustraliaThe adaptation of the lungs to air breathing at birth requires the fine orchestration of different processes to control lung morphogenesis and progenitor cell differentiation. However, there is little understanding of the role that epigenetic modifiers play in the control of lung development. We found that the histone methyl transferase Ezh2 plays a critical role in lung lineage specification and survival at birth. We performed a genome-wide transcriptome study combined with a genome-wide analysis of the distribution of H3K27 tri-methylation marks to interrogate the role of Ezh2 in lung epithelial cells. Lung cells isolated from Ezh2-deficient and control mice at embryonic day E16.5 were sorted into epithelial and mesenchymal populations based on EpCAM expression. This enabled us to dissect the transcriptional and epigenetic changes induced by the loss of Ezh2 specifically in the lung epithelium. Here we provide a detailed description of the analysis of the RNA-seq and ChIP-seq data, including quality control, read mapping, differential expression and differential binding analyses, as well as visualisation methods used to present the data. These data can be accessed from the Gene Expression Omnibus database (super-series accession number GSE57393).http://www.sciencedirect.com/science/article/pii/S2213596015001506 |
spellingShingle | Aliaksei Z. Holik Laura A. Galvis Aaron T.L. Lun Matthew E. Ritchie Marie-Liesse Asselin-Labat Transcriptome and H3K27 tri-methylation profiling of Ezh2-deficient lung epithelium Genomics Data |
title | Transcriptome and H3K27 tri-methylation profiling of Ezh2-deficient lung epithelium |
title_full | Transcriptome and H3K27 tri-methylation profiling of Ezh2-deficient lung epithelium |
title_fullStr | Transcriptome and H3K27 tri-methylation profiling of Ezh2-deficient lung epithelium |
title_full_unstemmed | Transcriptome and H3K27 tri-methylation profiling of Ezh2-deficient lung epithelium |
title_short | Transcriptome and H3K27 tri-methylation profiling of Ezh2-deficient lung epithelium |
title_sort | transcriptome and h3k27 tri methylation profiling of ezh2 deficient lung epithelium |
url | http://www.sciencedirect.com/science/article/pii/S2213596015001506 |
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