AI Article Synopsis
- DNA replication is hindered by various internal and external factors that can disrupt the replication process, activating a checkpoint response to protect the DNA.
- Mild replication stress may lead to cell cycle exit, preventing cells in the S/G2 phase from proceeding to mitosis by prematurely activating the anaphase promoting complex/cyclosome (APC/C).
- The reduction of APC/C inhibitor EMI1/FBXO5 levels, driven by FOXO-mediated inhibition of the transcription factor E2F1, is crucial for limiting the duration of reversible replication stress checkpoints, ultimately helping to sustain genomic stability.
Article Abstract
DNA replication is challenged by numerous exogenous and endogenous factors that can interfere with the progression of replication forks. Substantial accumulation of single-stranded DNA during DNA replication activates the DNA replication stress checkpoint response that slows progression from S/G2 to M phase to protect genomic integrity. Whether and how mild replication stress restricts proliferation remains controversial. Here, we identify a cell cycle exit mechanism that prevents S/G2 phase arrested cells from undergoing mitosis after exposure to mild replication stress through premature activation of the anaphase promoting complex/cyclosome (APC/C). We find that replication stress causes a gradual decrease of the levels of the APC/C inhibitor EMI1/FBXO5 through Forkhead box O (FOXO)-mediated inhibition of its transcription factor E2F1. By doing so, FOXOs limit the time during which the replication stress checkpoint is reversible and thereby play an important role in maintaining genomic stability.
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| http://dx.doi.org/10.1016/j.celrep.2020.108675 | DOI Listing |
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