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SMYD5 regulates H4K20me3-marked heterochromatin to safeguard ES cell self-renewal and prevent spurious differentiation

ABSTRACT: SMYD5 regulates H4K20me3-marked heterochromatin to safeguard ES cell self-renewal and prevent spurious differentiation

PROVIDER: PRJNA368813 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5198800.fastq.gz	Fastqsanger.gz
	SRR5198810.fastq.gz	Fastqsanger.gz
	SRR5198791.fastq.gz	Fastqsanger.gz
	SRR5198801.fastq.gz	Fastqsanger.gz
	SRR5198811.fastq.gz	Fastqsanger.gz

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SMYD5 regulates H4K20me3-marked heterochromatin to safeguard ES cell self-renewal and prevent spurious differentiation [RNA-Seq]

Project description:Epigenetic regulation of chromatin states is thought to control the self-renewal and differentiation of embryonic stem (ES) cells. However, the roles of repressive histone modifications such as trimethylated histone lysine 20 (H4K20me3) in pluripotency and development are largely unknown. Here, we show that the histone lysine methyltransferase SMYD5 mediates H4K20me3 at heterochromatin regions. Depletion of SMYD5 leads to compromised self-renewal, including dysregulated expression of OCT4 targets, and perturbed differentiation. SMYD5 bound regions are enriched with repetitive DNA elements. Knockdown of SMYD5 results in a global decrease of H4K20me3 levels, a redistribution of heterochromatin constituents including H3K9me3/2, G9a, and HP1α, and de-repression of endogenous retroelements. A loss of SMYD5-dependent silencing of heterochromatin nearby genic regions leads to upregulated expression of lineage-specific genes, thus contributing to the decreased self-renewal and accelerated differentiation of SMYD5-depeleted ES cells. Altogether, these findings implicate a role for SMYD5 in regulating ES cell self-renewal and H4K20me3-marked heterochromatin.

2017-06-12 | GSE94085 | GEO

SMYD5 regulates H4K20me3-marked heterochromatin to safeguard ES cell self-renewal and prevent spurious differentiation [ChIP-Seq]

2017-06-12 | GSE94033 | GEO

H4K20me3 methyltransferase SMYD5 controls heterochromatin and chromosome integrity during embryonic stem cell differentiation

Project description:Epigenetic regulation of chromatin states is thought to control gene expression programs during lineage specification. However, the roles of repressive histone modifications such as trimethylated histone lysine 20 (H4K20me3) in development and genome stability are largely unknown. Here, we show that depletion of SMYD5, a H4K20me3 methyltransferase, leads to decreased H4K20me3 and H3K9me3 ChIP-Seq levels, and de-repression of endogenous LTR/LINE elements during differentiation. SMYD5 depletion results in chromosomal aberrations and the formation of transformed cells that exhibit decreased H4K20me3 and H3K9me3 levels and an expression signature consistent with multiple human cancers. Moreover, dysregulated gene expression in SMYD5 cancer cells is associated with LTR/ERV elements and decreased H4K20me3. These findings implicate an important role for SMYD5 in maintaining chromosome integrity by regulating heterochromatin and repressing endogenous repetitive DNA elements during differentiation.

2018-02-13 | GSE94955 | GEO

H4K20me3 methyltransferase SMYD5 controls heterochromatin and chromosome integrity during embryonic stem cell differentiation [DNA-seq]

2018-03-14 | GSE95094 | GEO

SMYD5 regulates H4K20me3-marked heterochromatin to safeguard ES cell self-renewal and prevent spurious differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-06-12 | GSE94086 | GEO

Mus musculus

Project description:SMYD5 regulates H4K20me3-marked heterochromatin to safeguard ES cell self-renewal and prevent spurious differentiation [RNA-Seq]

| PRJNA368814 | ENA

Mus musculus

Project description:SMYD5 regulates H4K20me3-marked heterochromatin to safeguard ES cell self-renewal and prevent spurious differentiation [ChIP-Seq]

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ChIP-SEQ of H4K20me3 in BCSCsSETD4 and BCSCsGFP

Project description:We report the ChIP-SEQ results of H4K20me3 in BCSCsSETD4 and BCSCsGFP. To explore epigenetic regulation by H4K20me3 in BCSC quiescence, we performed chromatin immunoprecipitation sequencing (ChIP-seq) using BCSCsSETD4 and BCSCsGFP. Quiescent BCSCsSETD4 showed marked enrichment of H4K20me3 modifications relative to BCSCsGFP.

2019-10-25 | GSE123841 | GEO

SMYD5 catalyzes histone H3 lysine 36 trimethylation at promoters

Project description:Histone mark, one carrier of epigenetic information, regulates the gene expression in cells. Studies have shown that H3K36me3 is mainly catalyzed by SETD2 to be deposited at gene body regions in mammalian cells. Here, we profile the distributions of H3K36me3 in native cells and uncover that H3K36me3 is also enriched at the promoters beyond the gene body regions. We identify SMYD5 as one methyltransferase responsible for the enrichment of H3K36me3 at promoters. Through RNA polymerase II, SMYD5 is recruited to chromatin to regulate H3K36me3 and gene expression. The enzymatic activity of SMYD5 is dependent on its C-terminal glutamic acid rich domain. Depletion of C-terminal domain reduces the reestablishment of H3K36me3 at promoters when Smyd5 is over-expressed in Smyd5 knockout cells. Furthermore, elevated Smyd5 expression contributes to the tumorigenesis of liver hepatocellular carcinoma. Together, our study reveals SMYD5 as the H3K36me3 methyltransferase at promoters to regulate the gene expression, providing important insights into the localization and function of H3K36me3.

2022-04-26 | GSE184894 | GEO

Control of Pro-Inflammatory Gene Programs by Regulated Trimethylation and Demethylation of Histone H4K20

Project description:Regulation of genes that initiate and amplify inflammatory programs of gene expression is achieved by signal-dependent exchange of co-regulator complexes that function to read, write and erase specific histone modifications linked to transcriptional activation or repression. Here, we provide evidence for an unexpected role of trimethylated histone H4 lysine 20 (H4K20me3) as a repression checkpoint that restricts expression of toll like receptor 4 (TLR4) target genes in macrophages. H4K20me3 is deposited at the promoters of a subset of these genes by the SMYD5 histone methyltransferase through its association with NCoR co-repressor complexes. Signal-dependent erasure of H4K20me3 is required for effective gene activation and is achieved by NF-KB-dependent delivery of the histone demethylase PHF2. Liver X receptors antagonize TLR4-dependent gene activation by maintaining NCoR/SMYD5-mediated repression. These findings reveal a histone H4K20 tri-methylation/de-methylation strategy that integrates positive and negative signaling inputs that control immunity and homeostasis. mRNA profiling from thioglycollate-elicited mouse macrophages treated with siRNA for Control, Smyd5 and Phf2 for 48 hours followed by 4 hours of LPS treatment.

2012-07-04 | E-GEOD-39113 | biostudies-arrayexpress

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