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MORC2 promotes renal carcinogenesis via epigenetically downregulating DAPK1

ABSTRACT: MORC2 promotes renal carcinogenesis via epigenetically downregulating DAPK1

PROVIDER: PRJNA913012 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22764432_1.fastq.gz	Fastqsanger.gz
	SRR22764432_2.fastq.gz	Fastqsanger.gz
	SRR22764433_1.fastq.gz	Fastqsanger.gz
	SRR22764433_2.fastq.gz	Fastqsanger.gz
	SRR22764434_1.fastq.gz	Fastqsanger.gz

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MORC2 promotes renal carcinogenesis via epigenetically downregulating DAPK1

Project description:epigenetic regulation plays a vital role in renal carcinogenesis. Here，we found epigenetic regulator MORC2 promoted carcinogenesis in kidney. Mechanistically, MORC2 functioned as oncogene via epigenetically silencing canonical tumor suppressor DAPK1 in kidney. Therefore, aMORC2—DAPK1 pro—oncogenic axis was identified in kindey.

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ATAC-seq profiling of mutated MORC2 overexpression in MORC2-knocked-out HEK293T cells

Project description:We report an in vitro reconstitution of full-length MORC2, the most commonly mutated MORC member, linked to various cancers and neurological disorders. MORC2 possesses multiple DNA binding sites that undergo structural rearrangement upon DNA binding. MORC2 locks onto the DNA using its C-terminal domain (CTD) and acts as a sliding clamp. A conserved phosphate-interacting motif within the CTD was found to regulate ATP hydrolysis and cooperative DNA binding. Importantly, MORC2 mediates chromatin remodelling via ATP hydrolysis-dependent DNA compaction, regulated by the phosphorylation state of its CTD.

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H3K9me3 and MORC2 ChIP-seq profiling of wild-type and MORC2-knock-out HEK293T cells

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MORC2 phosphorylation fine tunes its DNA compaction activity

Project description:Variants in the poorly characterised oncoprotein, MORC2, a chromatin remodelling ATPase, lead to defects in epigenetic regulation and DNA damage response. MORC2 variants are associated with multiple cancers and neurological disorders1,2. The C-terminal domain (CTD) of MORC2 is often phosphorylated in DNA damage response and is known to induce cancer progression in in vivo and in vitro cancer models3-5. However, it remains unclear how MORC2 CTD and its phosphorylation impacts its chromatin remodelling activity. Here, we report a molecular characterisation of full-length, phosphorylated MORC2. We show that MORC2 preferentially binds open chromatin, has multiple DNA binding sites with varying affinities and acts as a DNA sliding clamp. We identified a phosphate interacting motif within the CTD that dictates ATP hydrolysis and cooperative DNA binding. The DNA binding impacts several structural domains within the N-terminal ATPase region. We provide the first visual proof that MORC2 induces chromatin remodelling through ATP hydrolysis-dependent DNA compaction, where the speed of compaction is affected by its phosphorylation state. Together, our results reveal that phosphorylation of MORC2 CTD modulates its chromatin remodelling and could be an attractive target for therapeutics.

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Assessing the genome-wide occupancy of MORC2

Project description:By comparing HeLa cells expressing V5 epitope-tagged MORC2 constructs, the goal of the experiment was to determine the genome-wide localisation of MORC2 in the presence or absence of the HUSH complex and upon inactivation of the CW domain. The occupancy of V5-MORC2 was also compared to that of endogenous TASOR.

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ATAC-seq profiling of MORC2 knock-out HEK293T cells

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Assessing the impact of loss of MORC2 on the transcriptome

Project description:By comparing HeLa cells lacking MORC2 generated through CRISPR/Cas9-mediated gene disruption to wild-type HeLa cells, the goal of the experiment was to determine the effect of loss of MORC2 on the transcriptome.

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Transcription profiling of rat renal carcinogenesis model - oxidative stress-induced

Project description:An iron chelate, ferric nitrilotriacetate (Fe-NTA), induces oxidative renal tubular damage that subsequently leads to renal cell carcinoma in rodents. Here we used gene expression microarrays to find target oncogenes in this model. Network analysis of the gene expression microarray data revealed the involvement of beta-catenin pathway in the induced cancers. Experiment Overall Design: Carcinogenesis protocol was performed using specific pathogen-free male Wistar rats or male F1 hybrid rats between Fischer344 and Brown-Norway strains. A total of 10 microarrays (Rat Genome 230 2.0; 31,999 genes; Affymetrix Inc., Santa Clara, CA) were used for the screening purpose; two for each group of untreated control, Fe-NTA treatment for 1 week, Fe-NTA treatment for 3 weeks, Fe-NTA-induced RCCs with neither peritoneal invasion nor metastasis and Fe-NTA-induced RCCs with pulmonarymetastasis.

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