期刊
CELL
卷 140, 期 5, 页码 678-691出版社
CELL PRESS
DOI: 10.1016/j.cell.2010.01.003
关键词
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资金
- National Institutes of Health (NIH) [GM07739, RR00862, RR022220, DP1DA026192, GM53122, GM53512]
- Damon Runyon Cancer Research Foundation
- Rockefeller University
- Starr Foundation
- New York State Department of Health [C023046]
- Howard Hughes Medical Institute
- Biotechnology and Biological Sciences Research Council UK
- British Heart Foundation
- Albert Einstein College of Medicine of Yeshiva University
- Biotechnology and Biological Sciences Research Council [BB/E009603/1] Funding Source: researchfish
- Medical Research Council [G1000801b, MC_U137961147, G1000801j] Funding Source: researchfish
- BBSRC [BB/E009603/1] Funding Source: UKRI
- MRC [MC_U137961147] Funding Source: UKRI
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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