Title: Chk1 inhibits E2F6 repressor function in response to replication stress to maintain cell-cycle transcription.
Authors: Bertoli C, Klier S, McGowan C, Wittenberg C, de Bruin RA.
This work reveals, for the first time, that the regular cell-cycle transcriptional program is part of the DNA replication checkpoint response in human cells and establishes the molecular mechanism involved. We show that maintaining high levels of G1/S cell-cycle transcription in response to replication stress contributes to two key functions of the DNA replication checkpoint response, namely, preventing genomic instability and cell death. Given the critical role of replication stress in oncogene transformation, a detailed understanding of the molecular mechanisms involved in the checkpoint response will contribute to a better insight into cancer development.