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The histone demethylase KDM5C regulates IRF transcriptional programming impacting dendritic cell population heterogeneity and function (RNA-seq)

ABSTRACT: The histone demethylase KDM5C regulates IRF transcriptional programming impacting dendritic cell population heterogeneity and function (RNA-seq)

PROVIDER: PRJNA1094398 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28506813_1.fastq.gz	Fastqsanger.gz
	SRR28506813_2.fastq.gz	Fastqsanger.gz
	SRR28506814_1.fastq.gz	Fastqsanger.gz
	SRR28506814_2.fastq.gz	Fastqsanger.gz
	SRR28506815_1.fastq.gz	Fastqsanger.gz

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The histone demethylase KDM5C regulates IRF transcriptional programming impacting dendritic cell population heterogeneity and function

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The histone demethylase KDM5C regulates IRF transcriptional programming impacting dendritic cell population heterogeneity and function (CUT&RUN)

Project description:The histone demethylase KDM5C regulates IRF transcriptional programming impacting dendritic cell population heterogeneity and function (CUT&RUN)

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The histone demethylase KDM5C regulates IRF transcriptional programming impacting dendritic cell population heterogeneity and function (CUT&RUN)

Project description:Functional and phenotypic heterogeneity of dendritic cells (DCs) plays a crucial role in facilitating the development of diverse immune responses essential for host protection. We found that KDM5C, a histone lysine demethylase, regulates conventional DC (cDC) and plasmacytoid DC (pDC) population heterogeneity and function. Mice deficient in KDM5C in DCs, have increased proportions of cDC2Bs and cDC1s, which was partly dependent on type I interferon and pDCs. Loss of KDM5C resulted in an increase in Ly6C- pDCs, which, compared to Ly6C+ pDCs, have limited ability to produce type I interferon and can more efficiently stimulate antigen-specific CD8 T cells. KDM5C-deficient DCs have increased expression of inflammatory genes, altered expression of lineage-specific genes, and reduced function. In response to Listeria infection, KDM5C-deficient mice mounted reduced CD8 responses due to decreased antigen presentation by cDC1s. Thus, KDM5C is a key regulator of DC heterogeneity and a critical driver functional properties of DCs.

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The histone demethylase KDM5C regulates IRF transcriptional programming impacting dendritic cell population heterogeneity and function (RNA-seq)

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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.

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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.

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The histone demethylase KDM5C regulates IRF transcriptional programming impacting dendritic cell population heterogeneity and function

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

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Transcriptional re-programming of primary human macrophages by IRF-3 and IRF-7

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The Kdm5c histone demethylase controls enhancer and promoter function.

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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.

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