Complete loss of H3K9 methylation dissolves mouse heterochromatin organization

Montavon, Thomas; Shukeir, Nicholas; Erikson, Galina; Engist, Bettina; Onishi-Seebacher, Megumi; Ryan, Devon; Musa, Yaarub; Mittler, Gerhard; Meyer, Alexandra Graff; Genoud, Christel; Jenuwein, Thomas

doi:10.1038/s41467-021-24532-8

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Complete loss of H3K9 methylation dissolves mouse heterochromatin organization

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Montavon, Thomas
Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Shukeir, Nicholas
Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Erikson, Galina
Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Engist, Bettina
Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Onishi-Seebacher, Megumi
Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Ryan, Devon
Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Musa, Yaarub
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Mittler, Gerhard
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Jenuwein, Thomas
Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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https://www.nature.com/articles/s41467-021-24532-8
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Montavon et al. 2021.pdf
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Citation

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.

Cite as: https://hdl.handle.net/21.11116/0000-0008-E840-A

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.