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p600 is a multifunctional protein implicated in cytoskeletal organization, integrin-mediated survival signaling, calcium-calmodulin signaling and the N-end rule pathway of ubiquitin-proteasome-mediated proteolysis. While  push , the  Drosophila  counterpart of  p600 , is dispensable for development up to adult stage, the role of  p600  has not been studied during mouse development. Here we generated  p600  knockout mice to investigate the in vivo functions of p600. Interestingly, we found that homozygous deletion of  p600  results in lethality between embryonic days 11.5 and 13.5 with severe defects in both embryo and placenta. Since  p600  is required for placental development, we performed conditional disruption of  p600 , which deletes selectively  p600  in the embryo but not in the placenta. The conditional mutant embryos survive longer than knockout embryos but ultimately die before embryonic day 14.5. The mutant embryos display severe cardiac problems characterized by ventricular septal defects and thin ventricular walls. These anomalies are associated with reduced activation of FAK and decreased expression of MEF2, which is regulated by FAK and plays a crucial role in cardiac development. Moreover, we observed pleiotropic defects in the liver and brain. In sum, our study sheds light on the essential roles of p600 in fetal development.

p600 Plays Essential Roles in Fetal Development