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  m6A RNA methylation of major satellite repeat transcripts facilitates chromatin association and RNA:DNA hybrid formation in mouse heterochromatin

Duda, K. J., Ching, R. W., Jerabek, L., Shukeir, N., Erikson, G., Engist, B., et al. (2021). m6A RNA methylation of major satellite repeat transcripts facilitates chromatin association and RNA:DNA hybrid formation in mouse heterochromatin. Nucleic Acids Research (London), 49, 5568-5587. doi:10.1093/nar/gkab364.

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 Creators:
Duda, Katarzyna J1, Author
Ching, Reagan W.1, Author              
Jerabek, Lisa1, Author
Shukeir, Nicholas1, Author              
Erikson, Galina1, Author
Engist, Bettina1, Author              
Onishi-Seebacher, Megumi1, Author              
Perrera, Valentina1, Author              
Richter, Florian2, Author
Mittler, Gerhard2, Author              
Fritz, Katharina3, Author
Helm, Mark3, Author
Knuckles, Philip3, Author
Bühler, Marc3, Author
Jenuwein, Thomas1, Author              
Affiliations:
1Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243644              
2Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_persistent22              
3External Organizations, ou_persistent22              

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 Abstract: Heterochromatin has essential functions in maintaining chromosome structure, in protecting genome integrity and in stabilizing gene expression programs. Heterochromatin is often nucleated by underlying DNA repeat sequences, such as major satellite repeats (MSR) and long interspersed nuclear elements (LINE). In order to establish heterochromatin, MSR and LINE elements need to be transcriptionally competent and generate non-coding repeat RNA that remain chromatin associated. We explored whether these heterochromatic RNA, similar to DNA and histones, may be methylated, particularly for 5-methylcytosine (5mC) or methyl-6-adenosine (m6A). Our analysis in mouse ES cells identifies only background level of 5mC but significant enrichment for m6A on heterochromatic RNA. Moreover, MSR transcripts are a novel target for m6A RNA modification, and their m6A RNA enrichment is decreased in ES cells that are mutant for Mettl3 or Mettl14, which encode components of a central RNA methyltransferase complex. Importantly, MSR transcripts that are partially deficient in m6A RNA methylation display impaired chromatin association and have a reduced potential to form RNA:DNA hybrids. We propose that m6A modification of MSR RNA will enhance the functions of MSR repeat transcripts to stabilize mouse heterochromatin.

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Language(s): eng - English
 Dates: 2021-05-172021-06-04
 Publication Status: Published in print
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 Rev. Type: Peer
 Identifiers: DOI: 10.1093/nar/gkab364
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Title: Nucleic Acids Research (London)
  Other : Nucleic Acids Res
Source Genre: Journal
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Publ. Info: Oxford : Oxford University Press
Pages: - Volume / Issue: 49 Sequence Number: - Start / End Page: 5568 - 5587 Identifier: ISSN: 0305-1048
CoNE: https://pure.mpg.de/cone/journals/resource/110992357379342