Global increase in replication fork speed during a p57KIP2-regulated erythroid cell fate switch

Cell cycle regulators are increasingly implicated in cell fate decisions such as the acquisition or loss of pluripotency and self-renewal potential. The cell cycle mechanisms that regulate these cell fate decisions are largely unknown. Here we studied an S phase- dependent cell fate switch, in which murine early erythroid progenitors transition in vivo from a self-renewal state into a phase of active erythroid gene transcription and concurrent maturational cell divisions. We found that progenitors are dependent on p57KIP2-mediated slowing of replication forks for self-renewal, a novel function for cyclin-dependent kinase (CDK) inhibitors.

Source: Experimental Hematology - August 22, 2017 Category: Hematology Authors: Merav Socolovsky, Yung Hwang, Melinda Futran, Daniel Hidalgo Source Type: research