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  Complete loss of H3K9 methylation dissolves mouse heterochromatin organization

Montavon, T., Shukeir, N., Erikson, G., Engist, B., Onishi-Seebacher, M., Ryan, D., et al. (2021). Complete loss of H3K9 methylation dissolves mouse heterochromatin organization. Nature Communications, 12: 4359. doi:10.1038/s41467-021-24532-8.

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Montavon, Thomas1, Author
Shukeir, Nicholas1, Author              
Erikson, Galina1, Author
Engist, Bettina1, Author              
Onishi-Seebacher, Megumi1, Author              
Ryan, Devon1, Author
Musa, Yaarub2, Author
Mittler, Gerhard2, Author              
Meyer, Alexandra Graff3, Author
Genoud, Christel3, 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_2243641              
3External Organizations, ou_persistent22              

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 Abstract: Histone H3 lysine 9 (H3K9) methylation is a central epigenetic modification that defines heterochromatin from unicellular to multicellular organisms. In mammalian cells, H3K9 methylation can be catalyzed by at least six distinct SET domain enzymes: Suv39h1/Suv39h2, Eset1/Eset2 and G9a/Glp. We used mouse embryonic fibroblasts (MEFs) with a conditional mutation for Eset1 and introduced progressive deletions for the other SET domain genes by CRISPR/Cas9 technology. Compound mutant MEFs for all six SET domain lysine methyltransferase (KMT) genes lack all H3K9 methylation states, derepress nearly all families of repeat elements and display genomic instabilities. Strikingly, the 6KO H3K9 KMT MEF cells no longer maintain heterochromatin organization and have lost electron-dense heterochromatin. This is a compelling analysis of H3K9 methylation-deficient mammalian chromatin and reveals a definitive function for H3K9 methylation in protecting heterochromatin organization and genome integrity.

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Language(s): eng - English
 Dates: 2021-07-16
 Publication Status: Published online
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 Rev. Type: Peer
 Identifiers: DOI: 10.1038/s41467-021-24532-8
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Title: Nature Communications
  Abbreviation : Nat. Commun.
Source Genre: Journal
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Publ. Info: London : Nature Publishing Group
Pages: - Volume / Issue: 12 Sequence Number: 4359 Start / End Page: - Identifier: ISSN: 2041-1723
CoNE: https://pure.mpg.de/cone/journals/resource/2041-1723