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H3K9me3-heterochromatin loss at protein-coding genes enables developmental lineage specification
Author(s) -
Dario Nicetto,
Greg Donahue,
Tanya Jain,
Tao Peng,
Simone Sidoli,
Lihong Sheng,
Thomas Montavon,
Justin S. Becker,
Jessica Grindheim,
Kimberly R. Blahnik,
Benjamin A. García,
Kai Tan,
Roberto Bonasio,
Thomas Jenuwein,
Kenneth S. Zaret
Publication year - 2019
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.aau0583
Subject(s) - heterochromatin , biology , heterochromatin protein 1 , chromatin , histone methyltransferase , epigenetics , histone , microbiology and biotechnology , histone h3 , methyltransferase , gene silencing , prc2 , cellular differentiation , gene , genetics , methylation
Reversing chromatin dynamics for development Compacted chromatin regions, marked by trimethylation of histone H3 at position lysine 9 (H3K9me3), occur at highly repeated DNA sequences, helping to suppress recombination and gene expression. Because pluripotent cells contain low levels of H3K9me3 heterochromatin relative to differentiated cells, it has been thought that an increase in such heterochromatin helps to define cell differentiation. Nicettoet al. used two independent methods to examine compacted heterochromatic domains and found that H3K9me3 compaction increased at protein-coding genes during early mouse organogenesis. During differentiation, these domains open up to allow cell-specific expression. Loss of heterochromatin by genetic inactivation of the H3K9me3 methyltransferases caused ectopic expression of cell-inappropriate genes and tissue pathology.Science , this issue p.294

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