TY - JOUR
T1 - High mobility group N proteins modulate the fidelity of the cellular transcriptional profile in a tissue- and variant-specific manner
AU - Kugler, Jamie E.
AU - Horsch, Marion
AU - Huang, Di
AU - Furusawa, Takashi
AU - Rochman, Mark
AU - Garrett, Lillian
AU - Becker, Lore
AU - Bohla, Alexander
AU - Hölter, Sabine M.
AU - Prehn, Cornelia
AU - Rathkolb, Birgit
AU - Racz, Ildikó
AU - Aguilar-Pimentel, Juan Antonio
AU - Adler, Thure
AU - Adamski, Jerzy
AU - Beckers, Johannes
AU - Busch, Dirk H.
AU - Eickelberg, Oliver
AU - Klopstock, Thomas
AU - Ollert, Markus
AU - Stog̈er, Tobias
AU - Wolf, Eckhard
AU - Wurst, Wolfgang
AU - Yildirim, Ali On̈der
AU - Zimmer, Andreas
AU - Gailus-Durner, Valérie
AU - Fuchs, Helmut
AU - De Angelis, Martin Hrabě
AU - Garfinkel, Benny
AU - Orly, Joseph
AU - Ovcharenko, Ivan
AU - Bustina, Michael
PY - 2013/6/7
Y1 - 2013/6/7
N2 - 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 Hmgn1tm1/tm1, Hmgn 3tm1/tm1, and Hmgn5tm1/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 Hmgntm1/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.Weconclude 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.
AB - 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 Hmgn1tm1/tm1, Hmgn 3tm1/tm1, and Hmgn5tm1/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 Hmgntm1/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.Weconclude 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.
UR - http://www.scopus.com/inward/record.url?scp=84878750993&partnerID=8YFLogxK
U2 - 10.1074/jbc.M113.463315
DO - 10.1074/jbc.M113.463315
M3 - Article
C2 - 23620591
AN - SCOPUS:84878750993
SN - 0021-9258
VL - 288
SP - 16690
EP - 16703
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 23
ER -