RT Journal
A1 Al Adhami, Hala
A1 Evano, Brendan
A1 Le Digarcher, Anne
A1 Gueydan, Charlotte
A1 Dubois, Emeric
A1 Parrinello, Hugues
A1 Dantec, Christelle
A1 Bouschet, Tristan
A1 Varrault, Annie
A1 Journot, Laurent
T1 A systems-level approach to parental genomic imprinting: the imprinted gene network includes extracellular matrix genes and regulates cell cycle exit and differentiation
JF Genome Research 
JO Genome Research 
YR 2015 
FD March 01 
VO 25 
IS 3 
SP 353 
OP 367 
DO 10.1101/gr.175919.114 
UL http://genome.cshlp.org/content/25/3/353.abstract 
AB Genomic imprinting is an epigenetic mechanism that restrains the expression of ∼100 eutherian genes in a parent-of-origin-specific manner. The reason for this selective targeting of genes with seemingly disparate molecular functions is unclear. In the present work, we show that imprinted genes are coexpressed in a network that is regulated at the transition from proliferation to quiescence and differentiation during fibroblast cell cycle withdrawal, adipogenesis in vitro, and muscle regeneration in vivo. Imprinted gene regulation is not linked to alteration of DNA methylation or to perturbation of monoallelic, parent-of-origin-dependent expression. Overexpression and knockdown of imprinted gene expression alters the sensitivity of preadipocytes to contact inhibition and adipogenic differentiation. In silico and in cellulo experiments showed that the imprinted gene network includes biallelically expressed, nonimprinted genes. These control the extracellular matrix composition, cell adhesion, cell junction, and extracellular matrix-activated and growth factor–activated signaling. These observations show that imprinted genes share a common biological process that may account for their seemingly diverse roles in embryonic development, obesity, diabetes, muscle physiology, and neoplasm.