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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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Assessing the genome-wide occupancy of MORC2

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Assessing the impact of loss of MORC2 on the transcriptome

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

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DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex

Project description:The human silencing hub (HUSH) complex binds to transcripts of LINE-1 retrotransposons (L1s) and other genomic repeats, recruiting MORC2 and other effectors to remodel chromatin. However, how HUSH and MORC2 operate alongside DNA methylation, a central epigenetic regulator of repeat transcription, remains poorly understood. Here we interrogate this relationship in human neural progenitor cells (hNPCs), a somatic model of brain development that tolerates removal of DNA methyltransferase DNMT1. Upon loss of MORC2 or HUSH subunit TASOR in hNPCs, L1s remain silenced by robust promoter methylation. However, genome demethylation and activation of evolutionarily-young L1s attracts MORC2 binding. Simultaneous depletion of DNMT1 and MORC2 causes massive accumulation of L1 transcripts. We identify the same mechanistic hierarchy at pericentromeric α-satellites and clustered protocadherin genes, repetitive elements important for chromosome structure and neurodevelopment respectively. Our data delineate the independent epigenetic control of repeats in somatic cells, with implications for understanding the vital functions of HUSH-MORC2 in hypomethylated contexts throughout human development.

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DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [CUT&RUN]

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DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [Bulk RNA-seq]

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DNA methylation status determines the sensitivity of repeats to restriction by the HUSH-MORC2 complex [ONT cDNA sequencing]

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