Propagation of Adipogenic Signals through an Epigenomic Transition State

ABSTRACT: The transcriptional mechanisms by which temporary exposure to developmental signals instigates adipocyte differentiation are unknown. During early adipogenesis, we find transient enrichment of the glucocorticoid receptor (GR), CCAAT/enhancer binding protein b (CEBPb), p300, mediator subunit 1, and histone H3 acetylation near genes involved in cell proliferation, development and differentiation, including the gene encoding the master regulator of adipocyte differentiation, peroxisome proliferator activated receptor g2 (PPARg2). Occupancy and enhancer function are triggered by adipogenic signals, and diminish upon their removal. GR, which is required for adipogenesis but need not be active in the mature adipocyte, transiently functions with other enhancer proteins to propagate a new program

ORGANISM(S): Mus musculus

SUBMITTER: David Steger 

PROVIDER: E-GEOD-21898 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress