GSE104452
Gcn5 regulates FGF signaling outputs through c-Myc during early differentiation of embryoid bodies [ChIP-Seq]
Precise control of gene expression during development is orchestrated by transcription factors and co-regulators including chromatin modifiers.  How particular chromatin modifying enzymes affect specific developmental processes is not well defined. Here we report that Gcn5, a HAT essential for embryonic development, is largely required for c-MYC target gene transcription downstream of FGF signaling in early embryoid bodies (EBs). Gcn5 null EBs display deficient activation of ERK and p38, disorganized cytoskeletal networks, and compromised capacity to differentiate toward mesodermal and endodermal lineages. These findings establish a regulatory role for Gcn5 in execution of a critical signaling pathway during early development. Overall design: Day 5 embryoibodies (EBs) derived from Gcn5fx/fx (4_1, 6_1) and Gcn5-/- (4_C2, 6_C4) ES cells were subject to H3K9ac ChIP-seq experiments, in order to examine the changes in genomewide distribution of H3K9ac upon Gcn5 loss at early differentiation stage. ChIP DNA from 4 independent replicative experiments, including 2 replicates for each isolate pair (Gcn5fx/fx and Gcn5-/-), were used for deep sequencing.