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

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

PROVIDER: PRJNA665179 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12696911.fastq.gz	Fastqsanger.gz
	SRR12696912.fastq.gz	Fastqsanger.gz
	SRR12696913.fastq.gz	Fastqsanger.gz
	SRR12696914.fastq.gz	Fastqsanger.gz
	SRR12696915.fastq.gz	Fastqsanger.gz

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

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

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

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

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

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

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

| S-EPMC7846778 | biostudies-literature

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

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

2020-11-24 | GSE158406 | GEO

Comparative methylomics reveals gene-body H3K36me3 in Drosophila predicts DNA methylation and CpG landscapes in other invertebrates

Project description:Here, we demonstrate that Nematostella vectensis, Ciona intestinalis, Apis mellifera, and B. mori, show two distinct populations of genes differentiated by gene-body CpG density. Genome-scale DNA methylation profiles for A. mellifera spermatozoa reveal CpG-poor genes are methylated in the germ line, as predicted by the depletion of CpGs. We find an evolutionarily conserved distinction between CpG-poor and -rich genes: the former are associated with basic biological processes, the latter with more specialized functions. This distinction is strikingly similar to that recently observed between euchromatin-associated genes in Drosophila that contain intragenic histone 3 lysine 36 trimethylation (H3K36me3) and those that do not, even though Drosophila doesnât display CpG density bimodality or methylation. We confirm that a significant number of CpG-poor genes in N. vectensis, C. intestinalis, A. mellifera and B. mori are orthologs of H3K36me3- rich genes in Drosophila. We propose that over evolutionary time, gene-body H3K36me3 has influenced gene-body DNA methylation levels, and consequently the gene-body CpG density bimodality characteristic of invertebrates that harbor CpG methylation.

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Comparative methylomics reveals gene-body H3K36me3 in Drosophila predicts DNA methylation and CpG landscapes in other invertebrates

Project description:Here, we demonstrate that Nematostella vectensis, Ciona intestinalis, Apis mellifera, and B. mori, show two distinct populations of genes differentiated by gene-body CpG density. Genome-scale DNA methylation profiles for A. mellifera spermatozoa reveal CpG-poor genes are methylated in the germ line, as predicted by the depletion of CpGs. We find an evolutionarily conserved distinction between CpG-poor and -rich genes: the former are associated with basic biological processes, the latter with more specialized functions. This distinction is strikingly similar to that recently observed between euchromatin-associated genes in Drosophila that contain intragenic histone 3 lysine 36 trimethylation (H3K36me3) and those that do not, even though Drosophila doesnM-CM-"M-BM-^@M-BM-^Yt display CpG density bimodality or methylation. We confirm that a significant number of CpG-poor genes in N. vectensis, C. intestinalis, A. mellifera and B. mori are orthologs of H3K36me3- rich genes in Drosophila. We propose that over evolutionary time, gene-body H3K36me3 has influenced gene-body DNA methylation levels, and consequently the gene-body CpG density bimodality characteristic of invertebrates that harbor CpG methylation. Examination of DNA methylation in Apis Mellifera sperm

2011-06-16 | E-GEOD-29982 | biostudies-arrayexpress

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