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Expression data from Ezh2 epithelial knock-out mouse lungs at E14.5

ABSTRACT: Ezh2 epigenetically suppresses developmentally-regulated genes. Ezh2 is highly expressed during development, including in the lung. We knocked out Ezh2 in the developing lung epithelium using a Shh-cre driver which is active in foregut endoderm prior to lung morphogenesis. Many developmentally regulated genes became derepressed in the mutant lungs, leading to defects in lung development. Microarray analysis of genes upregulated in Ezh2 epithelial knock-out mouse lungs compared to Shh-cre controls.

ORGANISM(S): Mus musculus

PROVIDER: GSE60660 | GEO | 2015/02/04

SECONDARY ACCESSION(S): PRJNA259208

REPOSITORIES: GEO

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Expression data from Ezh2 epithelial knock-out mouse lungs at E14.5

Project description:Ezh2 epigenetically suppresses developmentally-regulated genes. Ezh2 is highly expressed during development, including in the lung. We knocked out Ezh2 in the developing lung epithelium using a Shh-cre driver which is active in foregut endoderm prior to lung morphogenesis. Many developmentally regulated genes became derepressed in the mutant lungs, leading to defects in lung development. Microarray analysis of genes upregulated in Ezh2 epithelial knock-out mouse lungs compared to Shh-cre controls. We generated Ezh2 epithelial mutant lungs by crossing the Ezh2-floxed line (Su et al., 2003) with the Shh-cre line (Harfe et al., 2004). We isolated RNA from whole mouse lungs at embryonic day 14.5 from 4 Shh-cre:Ezh2-flox/flox embryos (M1-M4) and 4 Shh-cre embryos (C1-C4). Littermates are as follows: C1+C2; C3+C4; M1+M2; M3+M4.

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Whole lung transcriptome from lung epithelial IRE1α knockout mice

Project description:This experiment sought to characterize the whole lung transcriptional changes induced by loss of IRE1a function in the lung epithelium. Mice were Shh(Cre/+) IRE1a(fl/fl) on the C57BL/6 background, and had loss of IRE1a function in the epithelium based on XBP1 splicing activity. Lungs from uninjured mice were harvested, flash-frozen, homogenized, and RNA isolated by Trizol extraction.

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Project description:Gene expression (RNA-seq) and H3K27me3 binding (ChIP-seq) profiling of wild type and Ezh2-deficient mouse lung epithelium. Lungs from wild type and Ezh2-deficient mice (Ezh2 deletion is specific to lung epithelium) were collected at day e16.5. Lung cells were separated into epithelial and stromal populations based on EpCAM expression. Epithelial cells were profiled for both gene expression (Total RNA-seq) and H3K27me3 binding (ChIP-seq). Additionally, stromal cells were also profiled for gene expression.

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Project description:To identify genes expressed during initiation of lung organogenesis, we generated transcriptional profiles of the prospective lung region of the mouse foregut (mid-foregut) microdissected from embryos at three developmental stages between embryonic day 8.5 (E8.5) and E9.5. This period spans from lung specification of foregut cells to the emergence of the primary lung buds. We identified a number of known and novel genes that are temporally regulated as the lung bud forms. Genes that regulate transcription, including DNA binding factors, co-factors, and chromatin remodeling genes, are the main functional groups that change during lung bud formation. Members of key developmental transcription and growth factor families, not previously described to participate in lung organogenesis, are expressed in the mid-foregut during lung bud induction. These studies also show early expression in the mid-foregut of genes that participate in later stages of lung development. This characterization of the mid-foregut transcriptome provides new insights into molecular events leading to lung organogenesis. Three samples (developmental stages), three biological replicates (5-10 pooled mid-foreguts)

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