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Activation of Xist by An Evolutionarily Conserved Function of the KDM5C Demethylase

ABSTRACT: Activation of Xist by An Evolutionarily Conserved Function of the KDM5C Demethylase

PROVIDER: PRJNA379738 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5351580.fastq.gz	Fastqsanger.gz
	SRR5351590.fastq.gz	Fastqsanger.gz
	SRR5351581.fastq.gz	Fastqsanger.gz
	SRR5351591.fastq.gz	Fastqsanger.gz
	SRR5351582.fastq.gz	Fastqsanger.gz

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Activation of Xist by An Evolutionarily Conserved Function of the KDM5C Demethylase

Project description:We performed Kdm5c (Smcx) ChIP-Seq in del_Tsix XY mouse epiblast cells with two genotypes: Smcx-WT and Smcx-KO

2022-04-14 | GSE96740 | GEO

Activation of Xist by An Evolutionarily Conserved Function of the KDM5C Demethylase

Project description:X-inactivation, which equalizes X-linked gene expression between the mammalian sexes, occurs due to the higher expression in females of the X-linked Kdm5c gene.

2022-04-14 | GSE96797 | GEO

Activation of Xist by an evolutionarily conserved function of KDM5C demethylase.

Project description:XX female and XY male therian mammals equalize X-linked gene expression through the mitotically-stable transcriptional inactivation of one of the two X chromosomes in female somatic cells. Here, we describe an essential function of the X-linked homolog of an ancestral X-Y gene pair, Kdm5c-Kdm5d, in the expression of Xist lncRNA, which is required for stable X-inactivation. Ablation of Kdm5c function in females results in a significant reduction in Xist RNA expression. Kdm5c encodes a demethylase that enhances Xist expression by converting histone H3K4me2/3 modifications into H3K4me1. Ectopic expression of mouse and human KDM5C, but not the Y-linked homolog KDM5D, induces Xist in male mouse embryonic stem cells (mESCs). Similarly, marsupial (opossum) Kdm5c but not Kdm5d also upregulates Xist in male mESCs, despite marsupials lacking Xist, suggesting that the KDM5C function that activates Xist in eutherians is strongly conserved and predates the divergence of eutherian and metatherian mammals. In support, prototherian (platypus) Kdm5c also induces Xist in male mESCs. Together, our data suggest that eutherian mammals co-opted the ancestral demethylase KDM5C during sex chromosome evolution to upregulate Xist for the female-specific induction of X-inactivation.

| S-EPMC9095838 | biostudies-literature

The Kdm5c histone demethylase controls enhancer and promoter function.

Project description:Here, we show that the Kdm5c/Smcx member of the Jarid1 family of H3K4 demethylases is recruited to both enhancer and core promoter elements in ES and neuronal progenitor cells (NPC). Knockdown of Kdm5c deregulates transcription via a local increase in H3K4me3. While at core promoters the function of Kdm5c is to restrict transcription, loss of Kdm5c impairs enhancer function. Remarkably, an impaired enhancer function activates promoter activity from Kdm5c-bound intergenic regions. Our results demonstrate that the Kdm5c demethylase plays a crucial role in the functional identity and discrimination of enhancers and core promoters. We speculate that this is related to recruitment of H3K4me3 binders like the TFIID and NURF complexes6-8. Providing functional identity to genomic regions through balancing enzymes that deposit and remove histone modifications may prove to be a general epigenetic mechanism for the functional indexing of eukaryotic genomes. Examination of the KDM5C binding sites in mouse embryonic stem cells and in neuronal progenitor cells. Effect of KDM5C knock down on H3K4me3 and H3K4me1 levels and gene expression.

2013-04-01 | E-GEOD-34975 | biostudies-arrayexpress

The Histone Demethylase KDM5C Functions as a Tumor Suppressor in AML by Repression of B ivalently M arked Immature Genes

Project description:To uncover novel epigenetic regulators in AML, we performed an in vivo short hairpin RNA (shRNA) screen in the context of Cebpa mutant AML. This led to the identification of the Histone 3 Lysine 4 (H3K4) demethylase, KDM5C, as a novel tumor suppressor in AML. KDM5C potentially functions as a transcriptional repressor via its demethylase activity at promoters, and dysregulation could therefore have widespread consequences. Here, we found that reduced Kdm5c/KDM5C expression is associated with accelerated growth in both human and murine AML cell lines. In vivo, Kdm5c knockdown in a Cebpa mutant AML mouse model resulted in a more aggressive, immature and short-latency phenotype. Mechanistically, we show that knockdown of Kdm5c increased H3K4me3 globally. This translated into the up-regulation of a group of bivalently marked immature genes, resulting in a de-differentiation phenotype which could be reversed by modulating levels of pro-differentiation factors. Finally, we demonstrated that low levels of KDM5C were associated with a decrease in long-term disease-free survival, specifically in female patients. This emphasizes the clinical relevance of our findings and identifies KDM5C as a novel female-biased tumor suppressor in AML.

2023-03-10 | PXD016568 | Pride

Mus musculus

Project description:Activation of Xist by An Evolutionarily Conserved Function of the KDM5C Demethylase

| PRJNA379739 | ENA

Mus musculus

Project description:Activation of Xist by An Evolutionarily Conserved Function of the KDM5C Demethylase

| PRJNA379480 | ENA

Activation of Xist by An Evolutionarily Conserved Function of the KDM5C Demethylase

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

2022-04-14 | GSE96798 | GEO

The Kdm5c histone demethylase controls enhancer and promoter function.

2013-04-01 | GSE34975 | GEO

Targeting transcriptional factor YY1 is synthetic lethal with loss of the histone demethylase KDM5C

Project description:In this study, we screened KDM5C-binding proteins and found that Yin Yang 1 (YY1) interacts with KDM5C. Interestingly, a synergistic antitumor effect was exerted when both KDM5C and YY1 were depleted, and targeting YY1 appeared to be a vulnerability in KDM5C-deficient cancer cells. Mechanistically, KDM5C is essential for global YY1 chromatin recruitment, especially at promoters. Moreover, an intact KDM5C JmjC domain but not KDM5C histone demethylase activity is required for KDM5C-mediated YY1 chromatin binding.Transcriptional profiling revealed that dual inhibition of KDM5C and YY1 led to significantly increased transcriptional repression of many cell cycle- and apoptosis-related genes. In summary, our work demonstrates a synthetic lethal interaction between YY1 and KDM5C and suggests a therapeutic vulnerability that can be targeted using combination therapies.

2024-06-28 | GSE270719 | GEO

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