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Genome-wide profiling of Kdm2a binding and H3K36me2 of hypoxia-cultured B cells derived from miR-155-sufficient and -deficient mice [ChIP-seq]

ABSTRACT: Genome-wide profiling of Kdm2a binding and H3K36me2 of hypoxia-cultured B cells derived from miR-155-sufficient and -deficient mice [ChIP-seq]

PROVIDER: PRJNA961712 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24301127_1.fastq.gz	Fastqsanger.gz
	SRR24301127_2.fastq.gz	Fastqsanger.gz
	SRR24301128_1.fastq.gz	Fastqsanger.gz
	SRR24301128_2.fastq.gz	Fastqsanger.gz
	SRR24301129_1.fastq.gz	Fastqsanger.gz

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Genome-wide profiling of Kdm2a binding and H3K36me2 of hypoxia-cultured B cells derived from miR-155-sufficient and -deficient mice [ChIP-seq]

Project description:To investigate the impact caused by miR-155 ablation, B cells from miR-155-sufficient and -deficient mice were cultured in hypoxic conditions and analyzed for profiling the binding of a miR-155 target, Kdm2a, to genomic loci and the distribution pattern of H3K36me2, which Kdm2a demethylates.

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The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [ChIP-seq]

Project description:To investigate how KDM2A regulates downstream genes and affects NPC function and the role of KDM2A in histone methylation, we performed KDM2A and H3K36me2 ChIP-Seq. By analyzing both datasets together, we identified 2,051 overlapping peaks that were shared by both KDM2A and H3K36me2, The enriched genes were found to be associated with generating neurons, central nervous system development and cell proliferation. Furthermore, disease enrichment analysis revealed significant associations with ASD, ID and other neurodevelopmental disorders, indicating KDM2A's roles in neural development.

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The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment.

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The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [RNA-seq]

Project description:To explore how KDM2A regulates downstream genes and impacts NPC function, we generated KDM2A knockdown H9 ESC lines using shRNA lentivirus. We designed five siRNAs and selected the two most effective ones for shRNA creation, which were then packaged into shRNA lentivirus (sh1, sh4). Subsequently, we induced these cells into NPCs and cerebral organoids. Through RNA-seq and DEG analysis, we observed that DEGs in NPCs were associated with the MAPK signaling pathway, a finding also present in cerebral organoids. We conducted a disease enrichment analysis on the obtained gene lists, revealing enrichment in neurodevelopmental disorders such as intellectual disability (ID) and autism spectrum disorder (ASD). This finding indirectly suggests that KDM2A plays a role in early neurodevelopmental processes.

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The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [ChIP-seq]

Project description:The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [ChIP-seq]

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Project description:The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment [RNA-seq]

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Transcriptome analysis of histone demethylase Kdm2a knockout in mouse embryonic stem cells

Project description:H3K36 methylation plays an important role in gene regulation. The role of H3K36 demethylase Kdm2b has been well studied. However, the role of Kdm2a in embryonic stem cells are still unkonwn. To study the function of Kdm2a in embryonic stem cells. We used CRISPR-gRNA system to knockout Kdm2a. We analyzed the gene expression change and identified target genes and repeats of Kdm2a. We uncovered a novel role of Kdm2a in regulating gene expression in embryonic stem cells.

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Project description:The nucleosome acidic patch is a major interaction hub for chromatin, providing a platform for enzymes to dock and orient for nucleosome-targeted activities. In order to define the molecular basis of acidic patch recognition proteome-wide, we performed an amino acid resolution acidic patch interactome screen. We discovered that the histone H3 lysine 36 (H3K36) demethylase KDM2A, but not its closely related paralog, KDM2B, requires the acidic patch for nucleosome binding. These KDM2 family JumonjiC (JmjC) domain lysine demethylases are critical to heterochromatin formation and are commonly misregulated in cancer. Despite fundamental roles in transcriptional regulation in health and disease, the molecular mechanisms governing nucleosome substrate specificity of KDM2A/B, or any other JmjC lysine demethylases, remain unclear. We used a covalent JmjC inhibitor to solve cryo-EM structures of KDM2A and KDM2B trapped in action on the nucleosome. Our structures show that KDM2-nucleosome binding is paralog-specific and facilitated by dynamic nucleosomal DNA unwrapping and histone charge shielding that mobilize the H3K36 sequence for demethylation.

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KDM2A and KDM2B cooperatively protect a subset of CpG Islands from DNA methylation [RRBS]

Project description:In the mammalian genome, most CpGs are methylated, however, regions of the genome known as CpG islands (CGIs) are largely unmethylated, which are closely associated with modulating gene expression. The KDM2 proteins (KDM2A and KDM2B) are recruited via their ZF-CxxC domains to CGIs and mediate demethylation of H3K36me2 at these regions. However, the mechanism whether and how KDM2 proteins protect CGIs from DNA methylation remains unknown. Here, we report that depletion of each or both KDM2 proteins, or mutation JmjC domains of KDM2 proteins, leads to a modest increase of DNA methylation at CGIs, but a significant increase at CGI shores. Depletion of both KDM2 proteins shows most obvious increase of DNA methylation, indicating that KDM2A and KDM2B cooperatively regulate DNA methylation at CGIs. We further show that DNA methylation in the absence of KDM2 proteins show more obvious increase at a subset of CpG Islands such as non-marked and H3K27me3-only CGIs than other CpG Islands like bivalent and H3K4me3-only CGIs. Taken together, our finding reveals the role for KDM2 proteins in regulating DNA methylation at CGIs, and uncovers the mechanism by which complex chromatin state including histone modifications and CGI binding proteins synergistically protect CGIs from DNA methylation.

2025-12-22 | GSE180558 | GEO

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