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

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De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands. / Masalmeh, Roza H. Ali; Taglini, Francesca; Rubio-Ramon, Cristina et al.
In: Nature Communications, Vol. 12, No. 1, 694, 29.01.2021.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Masalmeh, RHA, Taglini, F, Rubio-Ramon, C, Musialik, KI, Higham, J, Davidson-Smith, H, Kafetzopoulos, I, Pawlicka, KP, Finan, HM, Clark, R, Wills, J, Finch, AJ, Murphy, L & Sproul, D 2021, 'De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands', Nature Communications, vol. 12, no. 1, 694. https://doi.org/10.1038/s41467-020-20716-w

APA

Masalmeh, R. H. A., Taglini, F., Rubio-Ramon, C., Musialik, K. I., Higham, J., Davidson-Smith, H., Kafetzopoulos, I., Pawlicka, K. P., Finan, H. M., Clark, R., Wills, J., Finch, A. J., Murphy, L., & Sproul, D. (2021). De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands. Nature Communications, 12(1), Article 694. https://doi.org/10.1038/s41467-020-20716-w

Vancouver

Masalmeh RHA, Taglini F, Rubio-Ramon C, Musialik KI, Higham J, Davidson-Smith H et al. De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands. Nature Communications. 2021 Jan 29;12(1):694. doi: 10.1038/s41467-020-20716-w

Author

Masalmeh, Roza H. Ali ; Taglini, Francesca ; Rubio-Ramon, Cristina et al. / De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands. In: Nature Communications. 2021 ; Vol. 12, No. 1.

Bibtex

@article{af4e6d553e244022923dc8e7560f78fb,
title = "De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands",
abstract = "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.",
author = "Masalmeh, {Roza H. Ali} and Francesca Taglini and Cristina Rubio-Ramon and Musialik, {Kamila I.} and Jonathan Higham and Hazel Davidson-Smith and Ioannis Kafetzopoulos and Pawlicka, {Kamila P.} and Finan, {Hannah M.} and Richard Clark and Jimi Wills and Finch, {Andrew J.} and Lee Murphy and Duncan Sproul",
year = "2021",
month = jan,
day = "29",
doi = "10.1038/s41467-020-20716-w",
language = "English",
volume = "12",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",
number = "1",

}

RIS

TY - JOUR

T1 - De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands

AU - Masalmeh, Roza H. Ali

AU - Taglini, Francesca

AU - Rubio-Ramon, Cristina

AU - Musialik, Kamila I.

AU - Higham, Jonathan

AU - Davidson-Smith, Hazel

AU - Kafetzopoulos, Ioannis

AU - Pawlicka, Kamila P.

AU - Finan, Hannah M.

AU - Clark, Richard

AU - Wills, Jimi

AU - Finch, Andrew J.

AU - Murphy, Lee

AU - Sproul, Duncan

PY - 2021/1/29

Y1 - 2021/1/29

N2 - 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.

AB - 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.

U2 - 10.1038/s41467-020-20716-w

DO - 10.1038/s41467-020-20716-w

M3 - Journal article

VL - 12

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

IS - 1

M1 - 694

ER -