Mammalian alteration/deficiency in activation 3 (Ada3) is essential for embryonic development and cell cycle progression.

ABSTRACT: Ada3 protein is an essential component of histone acetyl transferase containing coactivator complexes conserved from yeast to human. We show here that germline deletion of Ada3 in mouse is embryonic lethal, and adenovirus-Cre mediated conditional deletion of Ada3 in Ada3(FL/FL) mouse embryonic fibroblasts leads to a severe proliferation defect which was rescued by ectopic expression of human Ada3. A delay in G(1) to S phase of cell cycle was also seen that was due to accumulation of Cdk inhibitor p27 which was an indirect effect of c-myc gene transcription control by Ada3. We further showed that this defect could be partially reverted by knocking down p27. Additionally, drastic changes in global histone acetylation and changes in global gene expression were observed in microarray analyses

SUBMITTER: Mohibi S 

PROVIDER: S-EPMC3436190 | biostudies-literature | 2012 Aug

REPOSITORIES: biostudies-literature