HMGN1 modulates nucleosome occupancy and DNase I hypersensitivity at the CpG island promoters of embryonic stem cells.

Abstract	Chromatin structure plays a key role in regulating gene expression and embryonic differentiation; however, the factors that determine the organization of chromatin around regulatory sites are not fully known. Here we show that HMGN1, a nucleosome-binding protein ubiquitously expressed in vertebrate cells, preferentially binds to CpG island-containing promoters and affects the organization of nucleosomes, DNase I hypersensitivity, and the transcriptional profile of mouse embryonic stem cells and neural progenitors. Loss of HMGN1 alters the organization of an unstable nucleosome at transcription start sites, reduces the number of DNase I-hypersensitive sites genome wide, and decreases the number of nestin-positive neural progenitors in the subventricular zone (SVZ) region of mouse brain. Thus, architectural chromatin-binding proteins affect the transcription profile and chromatin structure during embryonic stem cell differentiation.
Authors	Tao Deng, Z Iris Zhu, Shaofei Zhang, Fenfei Leng, Srujana Cherukuri, Loren Hansen, Leonardo Mariño-Ramírez, Eran Meshorer, David Landsman, Michael Bustin
Journal	Molecular and cellular biology (Mol Cell Biol) Vol. 33 Issue 16 Pg. 3377-89 (Aug 2013) ISSN: 1098-5549 [Electronic] United States
PMID	23775126 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)
Chemical References	HMGN1 Protein Intermediate Filament Proteins Nerve Tissue Proteins Nes protein, mouse Nestin Nucleosomes Deoxyribonuclease I
Topics	Animals Brain (cytology) Cells, Cultured CpG Islands Deoxyribonuclease I (metabolism) Embryonic Stem Cells (cytology, metabolism) Gene Deletion Gene Expression Profiling Gene Expression Regulation, Developmental HMGN1 Protein (genetics, metabolism) Intermediate Filament Proteins (metabolism) Male Mice Nerve Tissue Proteins (metabolism) Nestin Neurons (cytology, metabolism) Nucleosomes (genetics, metabolism) Promoter Regions, Genetic

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