| Literature DB >> 23620591 |
Jamie E Kugler1, Marion Horsch2, Di Huang3, Takashi Furusawa1, Mark Rochman1, Lillian Garrett4, Lore Becker5, Alexander Bohla6, Sabine M Hölter4, Cornelia Prehn2, Birgit Rathkolb7, Ildikó Racz8, Juan Antonio Aguilar-Pimentel9, Thure Adler10, Jerzy Adamski11, Johannes Beckers12, Dirk H Busch13, Oliver Eickelberg6, Thomas Klopstock14, Markus Ollert15, Tobias Stöger6, Eckhard Wolf16, Wolfgang Wurst17, Ali Önder Yildirim6, Andreas Zimmer8, Valérie Gailus-Durner2, Helmut Fuchs2, Martin Hrabě de Angelis18, Benny Garfinkel19, Joseph Orly19, Ivan Ovcharenko3, Michael Bustin20.
Abstract
The nuclei of most vertebrate cells contain members of the high mobility group N (HMGN) protein family, which bind specifically to nucleosome core particles and affect chromatin structure and function, including transcription. Here, we study the biological role of this protein family by systematic analysis of phenotypes and tissue transcription profiles in mice lacking functional HMGN variants. Phenotypic analysis of Hmgn1(tm1/tm1), Hmgn3(tm1/tm1), and Hmgn5(tm1/tm1) mice and their wild type littermates with a battery of standardized tests uncovered variant-specific abnormalities. Gene expression analysis of four different tissues in each of the Hmgn(tm1/tm1) lines reveals very little overlap between genes affected by specific variants in different tissues. Pathway analysis reveals that loss of an HMGN variant subtly affects expression of numerous genes in specific biological processes. We conclude that within the biological framework of an entire organism, HMGNs modulate the fidelity of the cellular transcriptional profile in a tissue- and HMGN variant-specific manner.Entities:
Keywords: Chromatin; Chromosomes/Non-histone Chromosomal Proteins; Gene Regulation; HMG Proteins; Mouse Physiology; Transcriptomics; Transgenic Mice
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Year: 2013 PMID： 23620591 PMCID： PMC3675603 DOI： 10.1074/jbc.M113.463315
Source DB: PubMed Journal: J Biol Chem ISSN： 0021-9258 Impact factor: 5.157