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Postnatal SETD1B is essential for learning and the regulation of neuronal plasticity genes

ABSTRACT: Postnatal SETD1B is essential for learning and the regulation of neuronal plasticity genes

PROVIDER: PRJNA747832 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15184000.fastq.gz	Fastqsanger.gz
	SRR15184001.fastq.gz	Fastqsanger.gz
	SRR15184002.fastq.gz	Fastqsanger.gz
	SRR15184003.fastq.gz	Fastqsanger.gz
	SRR15184004.fastq.gz	Fastqsanger.gz

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Postnatal SETD1B is essential for learning and the regulation of neuronal plasticity genes [WT scRNA-seq]

Project description:Histone 3 lysine 4 methylation (H3K4me) is mediated by six different lysine methyltransferases. Amongst these enzymes SET domain containing 1b (SETD1B) has been linked to syndromic intellectual disability but its role in the postnatal brain has not been studied yet. Here we employ mice that lack Setd1b from excitatory neurons of the postnatal forebrain and combine neuron-specific ChIP-seq and RNA-seq approaches to elucidate its role in neuronal gene expression. We observe that SETD1B controls the expression of genes with a broad H3K4me3 peak at their promoters that represent neuronal enriched genes linked to learning and memory function. Comparative analysis to corresponding data from conditional Kmt2a and Kmt2b knockout mice suggests that this function is specific to SETD1B. Moreover, postnatal loss of Setd1b leads to severe learning impairment, suggesting that SETD1B-mediated regulation of H3K4me levels in postnatal neurons is critical for cognitive function.

2021-12-17 | GSE185182 | GEO

Postnatal SETD1B is essential for learning and the regulation of neuronal plasticity genes [WT scRNA-seq]

Project description:Postnatal SETD1B is essential for learning and the regulation of neuronal plasticity genes [WT scRNA-seq]

| PRJNA767875 | ENA

Postnatal SETD1B is essential for learning and the regulation of neuronal plasticity genes

Project description:We have analyzed changes in histone 3 lysine 4 methylation (H3K4me3 and H3K4me1), histone acetylation (H3K9ac and H3K27ac) and gene expression resulting from Setd1b knockdown in adult hippocampal CA neurons in mice. We implemented Cre/loxP-mediated conditional knockout strategy in order to knockdown this histone methyltransferase in excitatory forebrain neurons in adult mice.

2021-09-16 | GSE180326 | GEO

Comparative gene expression analysis in OCI-LY19 isogenic cell lines with SETD1B mutation or KMT2D+SETD1B double mutants.

Project description:The translocation t(14;18) activates BCL2 and is considered the initiating genetic lesion in most follicular lymphomas (FL). Surprisingly, FL patients fail to respond to the BCL2 inhibitor, Venetoclax. We show that mutations and deletions affecting the histone lysine methyltransferase SETD1B (KMT2G) occur in 7% of FLs and in 16% of diffuse large B cell lymphomas (DLBCL). Deficiency in SETD1B confers striking resistance to Venetoclaxand to an experimental MCL-1 inhibitor. SETD1B also acts as a tumor suppressor andcooperates with loss ofKMT2Din lymphoma development in vivo. Consistently, loss of SETD1B in human lymphomas typically coincides with loss of KMT2D. Mechanistically, SETD1B is required for the expression of several pro-apoptotic BCL2 family proteins. Conversely, inhibitors of the KDM5 histoneH3K4demethylases restore BIM and BIK expression and synergize with Venetoclax inSETD1B-deficient lymphomas.

2024-08-23 | GSE273152 | GEO

Postnatal expression of the lysine methyltransferase SETD1B is essential for learning and the regulation of neuron-enriched genes.

Project description:In mammals, histone 3 lysine 4 methylation (H3K4me) is mediated by six different lysine methyltransferases. Among these enzymes, SETD1B (SET domain containing 1b) has been linked to syndromic intellectual disability in human subjects, but its role in the mammalian postnatal brain has not been studied yet. Here, we employ mice deficient for Setd1b in excitatory neurons of the postnatal forebrain, and combine neuron-specific ChIP-seq and RNA-seq approaches to elucidate its role in neuronal gene expression. We observe that Setd1b controls the expression of a set of genes with a broad H3K4me3 peak at their promoters, enriched for neuron-specific genes linked to learning and memory function. Comparative analyses in mice with conditional deletion of Kmt2a and Kmt2b histone methyltransferases show that SETD1B plays a more pronounced and potent role in regulating such genes. Moreover, postnatal loss of Setd1b leads to severe learning impairment, suggesting that SETD1B-dependent regulation of H3K4me levels in postnatal neurons is critical for cognitive function.

| S-EPMC8724770 | biostudies-literature

H3K5me3 modifications in OCI-LY19 cells with and without SETD1B mutations.

2024-08-23 | GSE273154 | GEO

Postnatal expression of the lysine methyltransferase SETD1B is essential for learning and the regulation of neuron-enriched genes

Project description:In mammals histone 3 lysine 4 methylation (H3K4me) is mediated by six different lysine methyltransferases. Amongst these enzymes, SETD1B (SET domain containing 1b) has been linked to syndromic intellectual disability in human subjects, but its role in the mammalian postnatal brain has not been studied yet. Here, we employ mice deficient for Setd1b in excitatory neurons of the postnatal forebrain, and combine neuron-specific ChIP-seq and RNA-seq approaches to elucidate its role in neuronal gene expression. We observe that Setd1b controls the expression of a set of genes with a broad H3K4me3 peak at their promoters, enriched for neuron-specific genes linked to learning and memory function. Comparative analyses in mice with conditional deletion of Kmt2a and Kmt2b histone methyltransferases show that SETD1B plays a more pronounced and potent role in regulating such genes. Moreover, postnatal loss of Setd1b leads to severe learning impairment, suggesting that SETD1B-dependent regulation of H3K4me levels in postnatal neurons is critical for cognitive function.

| S-SCDT-EMBOJ-2020-106459 | biostudies-other

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [PBAT]

Project description:Histone 3 lysine 4 trimethylation (H3K4me3) is an epigenetic mark found at active gene promoters and CpG islands. H3K4me3 is essential for mammalian development, yet mechanisms underlying its genomic targeting are poorly understood. H3K4me3 methyltransferases SETD1B and MLL2 are essential for oogenesis. We investigated changes in H3K4me3 in Setd1b conditional knockout (cKO) GV oocytes using ultra-low input ChIP-seq, in complement to DNA methylation and gene expression analysis. Setd1b cKO oocytes showed a redistribution of H3K4me3, with a marked loss at active gene promoters associated with downregulated gene expression. Remarkably, many regions gained H3K4me3 in Setd1b cKOs, in particular those that were DNA hypomethylated, transcriptionally inactive and CpG-rich. All of these are hallmarks of MLL2 targets; thus, loss of SETD1B appears to enable enhanced MLL2 activity. Our work reveals two distinct, complementary mechanisms of genomic targeting of H3K4me3 in oogenesis, with SETD1B linked to transcriptional activity and MLL2 to CpG content.

2022-01-17 | GSE167986 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [RNA-seq]

2022-01-17 | GSE167984 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [ChIP-seq]

2022-01-17 | GSE167985 | GEO