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DOI	10.1126/science.aau0583
	H3K9me3-heterochromatin loss at protein-coding genes enables developmental lineage specification
	Nicetto D.; Donahue G.; Jain T.; Peng T.; Sidoli S.; Sheng L.; Montavon T.; Becker J.S.; Grindheim J.M.; Blahnik K.; Garcia B.A.; Tan K.; Bonasio R.; Jenuwein T.; Zaret K.S.
发表日期	2019
ISSN	0036-8075
起始页码	294
结束页码	297
卷号	363 期号:6424
英文摘要	Gene silencing by chromatin compaction is integral to establishing and maintaining cell fates. Trimethylated histone 3 lysine 9 (H3K9me3)–marked heterochromatin is reduced in embryonic stem cells compared to differentiated cells. However, the establishment and dynamics of closed regions of chromatin at protein-coding genes, in embryologic development, remain elusive. We developed an antibody-independent method to isolate and map compacted heterochromatin from low–cell number samples. We discovered high levels of compacted heterochromatin, H3K9me3-decorated, at protein-coding genes in early, uncommitted cells at the germ-layer stage, undergoing profound rearrangements and reduction upon differentiation, concomitant with cell type–specific gene expression. Perturbation of the three H3K9me3-related methyltransferases revealed a pivotal role for H3K9me3 heterochromatin during lineage commitment at the onset of organogenesis and for lineage fidelity maintenance. 2017 © The Authors, some rights reserved.
英文关键词	histone H3; histone; antibody; cell; developmental biology; embryonic development; gene expression; genetic engineering; pigment; protein; adult; animal tissue; Article; cell differentiation; controlled study; embryo; embryo development; endoderm; gene expression; germ layer; heterochromatin; histone methylation; liver development; mesoderm; mouse; nonhuman; organogenesis; priority journal; RNA sequence; animal; C57BL mouse; cell differentiation; cell lineage; chemistry; cytology; embryonic stem cell; female; gene expression regulation; gene silencing; genetics; heterochromatin; knockout mouse; liver cell; mammalian embryo; methylation; pancreas islet beta cell; Animals; Cell Differentiation; Cell Lineage; Embryo, Mammalian; Embryonic Stem Cells; Female; Gene Expression Regulation, Developmental; Gene Silencing; Germ Layers; Hepatocytes; Heterochromatin; Histones; Insulin-Secreting Cells; Methylation; Mice; Mice, Inbred C57BL; Mice, Knockout; Organogenesis
语种	英语
来源期刊	Science
文献类型	期刊论文
条目标识符	http://gcip.llas.ac.cn/handle/2XKMVOVA/244877
作者单位	Institute for Regenerative Medicine, University of Pennsylvania, Philadelphia, PA, United States; Penn Epigenetics Institute, University of Pennsylvania, Philadelphia, PA, United States; Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA, United States; Department of Biomedical and Health Informatics, Children’s Hospital of Philadelphia, Philadelphia, PA, United States; Division of Oncology, Center for Childhood Cancer Research, Children’s Hospital of Philadelphia, Philadelphia, PA, United States; Department of Biochemistry and Molecular Biophysics, University of Pennsylvania, Philadelphia, PA, United States; Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany; Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States
推荐引用方式 GB/T 7714	Nicetto D.,Donahue G.,Jain T.,et al. H3K9me3-heterochromatin loss at protein-coding genes enables developmental lineage specification[J],2019,363(6424).
APA	Nicetto D..,Donahue G..,Jain T..,Peng T..,Sidoli S..,...&Zaret K.S..(2019).H3K9me3-heterochromatin loss at protein-coding genes enables developmental lineage specification.Science,363(6424).
MLA	Nicetto D.,et al."H3K9me3-heterochromatin loss at protein-coding genes enables developmental lineage specification".Science 363.6424(2019).