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Distinct factors control histone variant H3.3 localization at specific genomic regions. 2010
Aaron D Goldberg, and
Laura A Banaszynski, and
Kyung-Min Noh, and
Peter W Lewis, and
Simon J Elsaesser, and
Sonja Stadler, and
Scott Dewell, and
Martin Law, and
Xingyi Guo, and
Xuan Li, and
Duancheng Wen, and
Ariane Chapgier, and
Russell C DeKelver, and
Jeffrey C Miller, and
Ya-Li Lee, and
Elizabeth A Boydston, and
Michael C Holmes, and
Philip D Gregory, and
John M Greally, and
Shahin Rafii, and
Chingwen Yang, and
Peter J Scambler, and
David Garrick, and
Richard J Gibbons, and
Douglas R Higgs, and
Ileana M Cristea, and
Fyodor D Urnov, and
Deyou Zheng, and
C David Allis
Laboratory of Chromatin Biology and Epigenetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
The incorporation of histone H3 variants has been implicated in the epigenetic memory of cellular state. Using genome editing with zinc-finger nucleases to tag endogenous H3.3, we report genome-wide profiles of H3 variants in mammalian embryonic stem cells and neuronal precursor cells. Genome-wide patterns of H3.3 are dependent on amino acid sequence and change with cellular differentiation at developmentally regulated loci. The H3.3 chaperone Hira is required for H3.3 enrichment at active and repressed genes. Strikingly, Hira is not essential for localization of H3.3 at telomeres and many transcription factor binding sites. Immunoaffinity purification and mass spectrometry reveal that the proteins Atrx and Daxx associate with H3.3 in a Hira-independent manner. Atrx is required for Hira-independent localization of H3.3 at telomeres and for the repression of telomeric RNA. Our data demonstrate that multiple and distinct factors are responsible for H3.3 localization at specific genomic locations in mammalian cells.
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Sonja Stadler, and
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Laura A Banaszynski, and
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Sonja Stadler, and
Scott Dewell, and
Martin Law, and
Xingyi Guo, and
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Ariane Chapgier, and
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Michael C Holmes, and
Philip D Gregory, and
John M Greally, and
Shahin Rafii, and
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Yi chuan = Hereditas,
