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Trends Genet. 2016 Jan;32(1):29-41. doi: 10.1016/j.tig.2015.11.001. Epub 2015 Dec 8.

H3K9me3-Dependent Heterochromatin: Barrier to Cell Fate Changes.

Author information

1
Institute for Regenerative Medicine, Epigenetics Program, and Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.
2
Institute for Regenerative Medicine, Epigenetics Program, and Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA. Electronic address: zaret@upenn.edu.

Abstract

Establishing and maintaining cell identity depends on the proper regulation of gene expression, as specified by transcription factors and reinforced by epigenetic mechanisms. Among the epigenetic mechanisms, heterochromatin formation is crucial for the preservation of genome stability and the cell type-specific silencing of genes. The heterochromatin-associated histone mark H3K9me3, although traditionally associated with the noncoding portions of the genome, has emerged as a key player in repressing lineage-inappropriate genes and shielding them from activation by transcription factors. Here we describe the role of H3K9me3 heterochromatin in impeding the reprogramming of cell identity and the mechanisms by which H3K9me3 is reorganized during development and cell fate determination.

KEYWORDS:

H3K9me3; cell identity; development; heterochromatin; reprogramming

PMID:
26675384
PMCID:
PMC4698194
DOI:
10.1016/j.tig.2015.11.001
[Indexed for MEDLINE]
Free PMC Article

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