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Jmjd2a and Jmjd2c regulate H3K9me3 and H3K36me3 at H3K4me3 positive transcription start sites being essential for ESC self-renewal and embryogenesis (ChIP-Seq)

ABSTRACT: We have characterized the role of the Jmjd2/Kdm4 proteins in embryonic stem cell (ESC) biology, histone methylation and gene regulation. The Jmjd2 proteins are H3K9/H3K36 histone demethylases and three Jmjd2 family members are expressed in ESCs: Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c/Gasc1. We find that specifically Jmjd2a and Jmjd2c exert redundant functions, which are essential for ESC self-renewal and early embryonic development. ChIP-seq studies show that Jmjd2a and Jmjd2c both localize to H3K4me3 marked regions, where they have general and widespread roles preventing the accumulation of especially H3K9me3, but also H3K36me3. Jmjd2 catalytic activity is required for ESC maintenance, and increased H3K9me3 levels in knockout ESCs compromise the expression of several Jmjd2a/c targets, including genes that are important for ESC self-renewal. Thus, continual removal of H3K9 promoter methylation by Jmjd2 demethylases represents a novel mechanism ensuring transcriptional competence and stability of the pluripotent cell identity.

ORGANISM(S): Mus musculus

PROVIDER: GSE64252 | GEO | 2016/05/09

SECONDARY ACCESSION(S): PRJNA270535

REPOSITORIES: GEO

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Jmjd2a and Jmjd2c regulate H3K9me3 and H3K36me3 at H3K4me3 positive TSSs being essential for ESC self-renewal and embryogenesis (microarray)

Project description:We have characterized the role of the Jmjd2/Kdm4 proteins in embryonic stem cell (ESC) biology, histone methylation and gene regulation. The Jmjd2 proteins are H3K9/H3K36 histone demethylases and three Jmjd2 family members are expressed in ESCs: Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c/Gasc1. We find that specifically Jmjd2a and Jmjd2c exert redundant functions, which are essential for ESC self-renewal and early embryonic development. ChIP-seq studies show that Jmjd2a and Jmjd2c both localize to H3K4me3 marked regions, where they have general and widespread roles preventing the accumulation of especially H3K9me3, but also H3K36me3. Jmjd2 catalytic activity is required for ESC maintenance, and increased H3K9me3 levels in knockout ESCs compromise the expression of several Jmjd2a/c targets, including genes that are important for ESC self-renewal. Thus, continual removal of H3K9 promoter methylation by Jmjd2 demethylases represents a novel mechanism ensuring transcriptional competence and stability of the pluripotent cell identity.

2016-05-09 | GSE64251 | GEO

The Demethylase JMJD2C/KDM4C Localizes to H3K4me3 Positive Transcription Start Sites (Affymetrix microarray analysis)

Project description:We have mapped transcriptional changes after depletion of the histone demethylases JMJD2C/GASC1/KDM4C and JMJD2A/KDM4A alone or in combination in the esophageal squamous carcinoma cell line, KYSE150. The KYSE150 cell line contains an amplification of the JMJD2C locus. RNA was extracted from KYSE150 cells transfected with shRNAs targeting JMJD2C and/or JMJD2A. The experiment was performed in triplicates and expression levels analyzed using Affymetrix microarrays.

2014-01-09 | E-GEOD-53892 | biostudies-arrayexpress

Jmjd2c/Kdm4c facilitates the assembly of essential enhancer-protein complexes at the onset of embryonic stem cell differentiation

Project description:Jmjd2/Kdm4 H3K9-demethylases cooperate in promoting mouse embryonic stem cell (ESC) identity. However, little is known about their importance at the exit of ESC pluripotency. Here, we uncover that Jmjd2c facilitates this process by stabilizing the assembly of Mediator-Cohesin complexes at lineage-specific enhancers. Functionally, we show that Jmjd2c is required in ESCs to initiate appropriate gene expression programs upon somatic multi-lineage differentiation. In the absence of Jmjd2c, differentiation is stalled at an early post-implantation epiblast-like stage, while Jmjd2c-knockout ESCs remain capable of forming extra-embryonic endoderm derivatives. Dissection of the underlying molecular basis revealed that Jmjd2c is re-distributed to lineage-specific enhancers during ESC priming for differentiation. Interestingly, Jmjd2c-bound enhancers are co-occupied by the H3K9-methyltransferase G9a/Ehmt2, independently of its H3K9-modifying activity. Loss of Jmjd2c abrogates G9a recruitment and furthermore destabilizes loading of the Mediator and Cohesin components Med1 and Smc1a at newly activated and poised enhancers in ESC-derived epiblast-like cells. These findings unveil Jmjd2c-G9a as novel enhancer-associated factors, and implicate Jmjd2c as a molecular scaffold for the assembly of essential enhancer-protein complexes with impact on timely gene activation.

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The Demethylase JMJD2C/KDM4C Localizes to H3K4me3 Positive Transcription Start Sites (Affymetrix microarray analysis)

2014-01-09 | GSE53892 | GEO

ChIP-Seq of Jmjd2a and Jmjd2c in B220+ B cells

Project description:Here we reported the Jmjd2a and Jmjd2c are co-targeted at the essential genes of mouse activating B220+ B cells. B cell activation programs transcription networks that subsequently induce plasma cell differentiation, but how histone demethylases participating in this process remains elusive. We found that histone demethylases Jmjd2a and Jmjd2c are expressed in Tfh-mediated signals stimulated mouse spelenic B220+ B cells. we then perform ChIP-seq by using anti-Jmjd2a and anti-Jmjd2c antibodies to identified the genes regulated by Jmjd2a and Jmjd2c and required for correct activation.

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Expression data of Jmjd2a and Jmjd2c-regulated genes in plasma cell differentiation

Project description:Base on the privious studie from our lab, we found the histone demethylases, Jmjd2a and Jmjd2c are upregulated in stimulated primary B cells, depletion of Jmjd2a and Jmjd2c in stimulated B cells resulted in failed activation of B cells. Owimg to the essential functions of Jmjd2a and Jmjd2c, We here applied loss of function approach, such as siRNA, to study the how Jmjd2a and Jmjd2c regulate plasma cell differentiation.

2020-01-01 | GSE99750 | GEO

The Demethylase JMJD2C/KDM4C Localizes to H3K4me3 Positive Transcription Start Sites (ChIP-seq KYSE150 cell line)

Project description:We have mapped binding sites for the histone demethylase, JMJD2C/KDM4C/GASC1, and the effect of JMJD2C depletion on H3K9me3 and H3K36me3 distributions in KYSE150 cells. The human esophageal carcinoma cell line, KYSE150, contains an amplification of the JMJD2C locus. ChIP-seq was performed using chromatin from control or JMJD2C-depleted KYSE150 cells and antibodies recognizing JMJD2C, H3K4me3, H3K9me3 or H3K36me3.

2014-01-09 | E-GEOD-53938 | biostudies-arrayexpress

The Demethylase JMJD2C/KDM4C Localizes to H3K4me3 Positive Transcription Start Sites (ChIP-seq MEFs)

Project description:We have mapped binding sites for the histone demethylase, Jmjd2c/Kdm4c/Gasc1, in mouse embryonic fibroblasts (MEFs) and the impact of Jmjd2c depletion on H3K9me3 and H3K36me3 distributions. ChIP-seq was performed using antibodies recognizing Jmjd2c, H3K9me3 or H3K36me3. Chromatin was obtained from conditional Jmjd2c knockout MEFs cultured in the absence or presence of OHT to induce activation of Cre recombinase and loss of Jmjd2c expression.

2014-01-09 | E-GEOD-53939 | biostudies-arrayexpress

The Demethylase JMJD2C/KDM4C Localizes to H3K4me3 Positive Transcription Start Sites (ChIP-seq MEFs)

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Project description:We have mapped binding sites for the histone demethylase, Jmjd2c/Kdm4c/Gasc1, in mouse embryonic stem cells (ESCs). ChIP-seq was performed using an antibody recognizing Jmjd2c. Chromatin was obtained from conditional Jmjd2c knockout ESCs cultured in the absence or presence of OHT to induce activation of Cre recombinase and loss of Jmjd2c expression.

2014-01-09 | E-GEOD-53936 | biostudies-arrayexpress

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