ABSTRACT
Cells regulate proliferation by entering and progressing through the cell cycle. Conversely, cell growth is arrested by exiting the cell cycle. A balance of extrinsic and intrinsic signals normally mediates progression through or exit from the cell cycle.1 When mitotic signals are received by cells, small proteins called cyclins are upregulated. These cyclins complex with cyclin dependent kinases, phosphorylate their targets, conse quentially driving cell cycle progression from G1 into S. DNA is replicated during S phase, and after another gap phase (G2) to ensure the fidelity of DNA replication and evaluate the permissiveness of the environment, the cell proceeds to divide in M phase. The resulting daughter cells can either continue to cycle by immediately reentering G l, or go on to be mitotically quiescent. Critical cell cycle checkpoints exist between Gl/S-phase and G2/M. Studies put emphasis on the Gl/S checkpoint, which commits the cell to cycle once it has been traversed. When considering the cell cycle of beta cells, which have been shown to have a very low level of replication, our critical interest focuses on factors that drive beta cells from quiescence and commit them to the cell cycle at the Gl/S checkpoint.
