NDLI: Quantitative Analysis of the Chromatin Proteome in Disease Reveals Remodeling Principles and Identifies High Mobility Group Protein B2 as a Regulator of Hypertrophic Growth

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Franklin, Sarah Chen, Haodong Mitchell-Jordan, Scherise Ren, Shuxun Wang, Yibin Vondriska, Thomas M.
Description	Country affiliation: United States Author Affiliation: Franklin S ( Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA. sfranklin@mednet.ucla.edu)
Abstract	A fundamental question in biology is how genome-wide changes in gene expression are enacted in response to a finite stimulus. Recent studies have mapped changes in nucleosome localization, determined the binding preferences for individual transcription factors, and shown that the genome adopts a nonrandom structure in vivo. What remains unclear is how global changes in the proteins bound to DNA alter chromatin structure and gene expression. We have addressed this question in the mouse heart, a system in which global gene expression and massive phenotypic changes occur without cardiac cell division, making the mechanisms of chromatin remodeling centrally important. To determine factors controlling genomic plasticity, we used mass spectrometry to measure chromatin-associated proteins. We have characterized the abundance of 305 chromatin-associated proteins in normal cells and measured changes in 108 proteins that accompany the progression of heart disease. These studies were conducted on a high mass accuracy instrument and confirmed in multiple biological replicates, facilitating statistical analysis and allowing us to interrogate the data bioinformatically for modules of proteins involved in similar processes. Our studies reveal general principles for global shifts in chromatin accessibility: altered linker to core histone ratio; differing abundance of chromatin structural proteins; and reprogrammed histone post-translational modifications. Using small interfering RNA-mediated loss-of-function in isolated cells, we demonstrate that the non-histone chromatin structural protein HMGB2 (but not HMGB1) suppresses pathologic cell growth in vivo and controls a gene expression program responsible for hypertrophic cell growth. Our findings reveal the basis for alterations in chromatin structure necessary for genome-wide changes in gene expression. These studies have fundamental implications for understanding how global chromatin remodeling occurs with specificity and accuracy, demonstrating that isoform-specific alterations in chromatin structural proteins can impart these features.
File Format	HTM / HTML
ISSN	15359476
e-ISSN	15359484
DOI	10.1074/mcp.M111.014258
Journal	Molecular & Cellular Proteomics
Issue Number	6
Volume Number	11
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2012-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Proteomics Cardiomegaly Metabolism Chromatin Assembly And Disassembly Chromatin Hmgb2 Protein Proteome Animals Cell Enlargement Cluster Analysis Gene Expression Regulation Gene Knockdown Techniques Hmgb1 Protein Genetics Mice Mice, Inbred Balb C Myocardium Pathology Rna Interference Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Medicine Analytical Chemistry Molecular Biology Biochemistry

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