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• W1591208124 abstract "The DNA replication checkpoint transcriptionally up-regulates genes that allow cells to adapt to and survive replication stress. Our results show that, in the fission yeast Schizosaccharomyces pombe , the replication checkpoint regulates the entire G1/S transcriptional program by directly regulating MBF (aka DSC1), the G1/S transcription factor. Instead of initiating a checkpoint-specific transcriptional program, the replication checkpoint targets MBF to maintain the normal G1/S transcriptional program during replication stress. We propose a mechanism for this regulation, based on in vitro phosphorylation of the Cdc10 subunit of MBF by the Cds1 replication-checkpoint kinase. Substitution of two potential phosphorylation sites with phospho-mimetic amino acids suffice to promote the checkpoint transcriptional program, suggesting that Cds1 phosphorylation directly regulates MBF-dependent transcription. The conservation of MBF between fission and budding yeast, and recent results implicating MBF as a target of the budding yeast replication checkpoint, suggest that checkpoint regulation of the MBF transcription factor may be a conserved strategy for coping with replication stress. Furthermore, the structural and regulatory similarity between MBF and E2F, the metazoan G1/S transcription factor, suggests that this checkpoint mechanism may be broadly conserved among eukaryotes. Our result shows that both the replication checkpoint and the S-phase DNA damage checkpoint are involved in activating MBF regulated S-phase gene transcription and that this coordinated transcriptional response is beneficial for survival duringreplication stress. I demonstrate that the beneficial role of the transcriptional response during checkpoint activation is mediated by three major MBF transcripts: cdc22, mrc1 and mik1 . Mrc1 dependent stabilization of stalled fork is important during S phase arrest. However, cells ability to prevent mitosis (Mik1 dependent) along with stable fork (Mrc1dependent) both are crucial for survival. Our data also suggest that the level of Cdc22 is a determining factor for replication checkpoint activation and when over-expressed can alleviate the effects not only in HU but also in MMS." @default.
• W1591208124 created "2016-06-24" @default.
• W1591208124 creator A5077112082 @default.
• W1591208124 date "2008-01-01" @default.
• W1591208124 modified "2023-09-23" @default.
• W1591208124 title "Checkpoint Regulation of S-Phase Transcription: A Dissertation" @default.
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