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De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (T7-DNMT3B ChIP-Rx_seq)

ABSTRACT: De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (T7-DNMT3B ChIP-Rx_seq)

PROVIDER: PRJNA665180 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12696919_1.fastq.gz	Fastqsanger.gz
	SRR12696919_2.fastq.gz	Fastqsanger.gz
	SRR12696920_1.fastq.gz	Fastqsanger.gz
	SRR12696920_2.fastq.gz	Fastqsanger.gz
	SRR12696921_1.fastq.gz	Fastqsanger.gz

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De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (T7-DNMT3B ChIP-Rx_seq)

Project description:The aberrant gain of DNA methylation at CpG islands (CGIs) is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CGIs are targeted by de novo DNA methyltransferases (DNMTs) in a sequence-specific manner but this has not been tested. Using ectopically integrated CGIs, we find that aberrantly methylated CGIs are subject to low levels of de novo DNMT activity in colorectal cancer cells. By delineating DNMT targets, we find that instead de novo DNMT activity is targeted primarily to CGIs marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CGIs are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNMT activity at CGIs in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.

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DNMT3B PWWP mutations cause hypermethylation of heterochromatin (T7-DNMT3B ChIP-seq)

Project description:The correct establishment of DNA methylation patterns is vital for mammalian development and is achieved by the de novo DNA methyltransferases DNMT3A and DNMT3B. DNMT3B localises to H3K36me3 at actively transcribing gene bodies through its PWWP domain. It also functions at heterochromatin through an unknown recruitment mechanism. Here we find that knockout of DNMT3B causes losses of methylation predominantly at H3K9me3-marked heterochromatin and that DNMT3B PWWP domain mutations or deletion result in striking increases of methylation in H3K9me3-marked heterochromatin. Removal of the N-terminal region of DNMT3B affects its ability to methylate H3K9me3-marked regions. This region of DNMT3B directly interacts with HP1-alpha and facilitates the bridging of DNMT3B with H3K9me3-marked nucleosomes in vitro. Our results suggest that DNMT3B is recruited to H3K9me3 marked heterochromatin in a PWWP-independent manner that is facilitated by the protein's N-terminus through an interaction with a key heterochromatin protein. More generally, we suggest that DNMT3B plays a role in DNA methylation homeostasis at heterochromatin, a process which is disrupted in cancer, aging and Immunodeficiency, Centromeric Instability and Facial Anomalies (ICF) syndrome.

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De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (H3K36me3 ChIP-Rx_seq)

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De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (RRBS)

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DNMT3B PWWP mutations cause hypermethylation of heterochromatin (T7-DNMT3B ChIP-seq)

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De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island

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De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (RRBS)

Project description:De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG island (RRBS)

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