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Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE114198 | GEO | 2018/10/31

REPOSITORIES: GEO

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H3K9me3-heterochromatin loss at protein-coding genes enables developmental lineage specification.

Project description:Gene silencing by chromatin compaction is integral to establishing and maintaining cell fates. Trimethylated histone 3 lysine 9 (H3K9me3)-marked heterochromatin is reduced in embryonic stem cells compared to differentiated cells. However, the establishment and dynamics of closed regions of chromatin at protein-coding genes, in embryologic development, remain elusive. We developed an antibody-independent method to isolate and map compacted heterochromatin from low-cell number samples. We discovered high levels of compacted heterochromatin, H3K9me3-decorated, at protein-coding genes in early, uncommitted cells at the germ-layer stage, undergoing profound rearrangements and reduction upon differentiation, concomitant with cell type-specific gene expression. Perturbation of the three H3K9me3-related methyltransferases revealed a pivotal role for H3K9me3 heterochromatin during lineage commitment at the onset of organogenesis and for lineage fidelity maintenance.

| S-EPMC6664818 | biostudies-literature

Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification (srHC-seq)

Project description:Domains of transcriptionally repressed heterochromatin, decorated by histone 3 lysine 9 trimethylation (H3K9me3), are reduced in embryonic stem cells compared to fully differentiated cells. However, the establishment and dynamics of closed regions of chromatin at protein coding genes, in natural embryologic development, has not been described. We developed a novel, antibody-independent method to isolate and map compacted heterochromatin from low cell number samples. Unexpectedly, we uncovered extensive high levels of H3K9me3-decorated, compacted heterochromatin at protein coding genes in early, uncommitted cells in the three germ layers, undergoing profound rearrangements and reduction upon differentiation, concomitant with cell type-specific gene expression. Perturbation of the three H3K9me3-related methyltransferases revealed that H3K9me3 heterochromatin is required to maintain cell lineage fidelity. We propose a key role for chromatin-based restriction of gene activity via H3K9me3 during embryologic development

2018-10-31 | GSE114197 | GEO

Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification (ChIP-Seq)

2018-10-31 | GSE114196 | GEO

Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification (RNA-Seq)

2018-10-31 | GSE114195 | GEO

Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification

Project description:Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification

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Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification (RNA-Seq)

Project description:Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification (RNA-Seq)

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Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification (ChIP-Seq)

Project description:Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification (ChIP-Seq)

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Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification (srHC-seq)

Project description:Loss of H3K9me3 heterochromatin at protein coding genes enables developmental lineage specification (srHC-seq)

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Mdig de-represses H19 large intergenic non-coding RNA (lincRNA) by down-regulating H3K9me3 and heterochromatin.

Project description:Mineral dust-induced gene (mdig) had been linked to the development of human lung cancers associated with environmental exposure to mineral dust, tobacco smoke or other carcinogens. In the present studies, we demonstrated that the overexpression of mdig in A549 adenocarcinomic human alveolar type II epithelial cells decreases the heterochromatin conformation of the cells and de-represses the transcription of genes in the tandemly repeated DNA regions. Although mdig can only cause a marginal decrease of the total histone H3 lysine 9 trimethylation (H3K9me3), a significant reduction of H3K9me3 in the promoter region of H19, the paternally imprinted but maternally expressed gene transcribing a large intergenic non-coding RNA (lincRNA), was observed in the cells with mdig overexpression. Silencing mdig by either shRNA or siRNA not only increased the level of H3K9me3 in the promoter region of H19 but also attenuated the transcription of H19 long non-coding RNA. Demethylation assays using immunoprecipitated mdig and histone H3 peptide substrate suggested that mdig is able to remove the methyl groups from H3K9me3. Clinically, we found that higher levels of mdig and H19 expression correlate with poorer survival of the lung cancer patients. Taken together, our results imply that mdig is involved in the regulation of H3K9me3 to influence the heterochromatin structure of the genome and the expression of genes important for cell growth or transformation.

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Transcriptional enhancers in protein-coding exons of vertebrate developmental genes.

Project description:Many conserved noncoding sequences function as transcriptional enhancers that regulate gene expression. Here, we report that protein-coding DNA also frequently contains enhancers functioning at the transcriptional level. We tested the enhancer activity of 31 protein-coding exons, which we chose based on strong sequence conservation between zebrafish and human, and occurrence in developmental genes, using a Tol2 transposable GFP reporter assay in zebrafish. For each exon we measured GFP expression in hundreds of embryos in 10 anatomies via a novel system that implements the voice-recognition capabilities of a cellular phone. We find that 24/31 (77%) exons drive GFP expression compared to a minimal promoter control, and 14/24 are anatomy-specific (expression in four anatomies or less). GFP expression driven by these coding enhancers frequently overlaps the anatomies where the host gene is expressed (60%), suggesting self-regulation. Highly conserved coding sequences and highly conserved noncoding sequences do not significantly differ in enhancer activity (coding: 24/31 vs. noncoding: 105/147) or tissue-specificity (coding: 14/24 vs. noncoding: 50/105). Furthermore, coding and noncoding enhancers display similar levels of the enhancer-related histone modification H3K4me1 (coding: 9/24 vs noncoding: 34/81). Meanwhile, coding enhancers are over three times as likely to contain an H3K4me1 mark as other exons of the host gene. Our work suggests that developmental transcriptional enhancers do not discriminate between coding and noncoding DNA and reveals widespread dual functions in protein-coding DNA.

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