Adenovirus Replaces Mitotic Checkpoint Controls

摘要: Infection with adenovirus triggers the cellular DNA damage response, elements of which include cell death and cycle arrest. Early adenoviral proteins, including E1B-55K E4orf3 inhibit signaling in response to damage. A fraction cells infected an mutant unable express genes appeared arrest a mitotic-like state. Cells early G1 were predisposed this state at late times infection. This arrested state, displays hallmarks mitotic catastrophe, was prevented by expression either or genes. However, virus-infected became trapped presence microtubule poison colcemid, suggesting that two viral proteins restrict entry into mitosis facilitate exit from order prevent arresting mitosis. The protein inappropriate through its interaction tumor suppressor p53. facilitated possibly mislocalizing functionally inactivating cyclin B1. When expressed noninfected cells, overcame caused degradation-resistant R42A B1 variant. IMPORTANCE are type 5 p53-dependent manner. prevents newly described activity for appears depend on between facilitates mitosis, altering intracellular distribution By preventing promoting these act