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Genes 2017, 8(1), 10;

Mec1/ATR, the Program Manager of Nucleic Acids Inc.

Department of Biochemistry and Molecular Biology, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA
Academic Editor: Eishi Noguchi
Received: 5 November 2016 / Revised: 19 December 2016 / Accepted: 22 December 2016 / Published: 28 December 2016
(This article belongs to the Special Issue DNA Replication Controls)
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Eukaryotic cells are equipped with surveillance mechanisms called checkpoints to ensure proper execution of cell cycle events. Among these are the checkpoints that detect DNA damage or replication perturbations and coordinate cellular activities to maintain genome stability. At the forefront of damage sensing is an evolutionarily conserved molecule, known respectively in budding yeast and humans as Mec1 (Mitosis entry checkpoint 1) and ATR (Ataxia telangiectasia and Rad3-related protein). Through phosphorylation, Mec1/ATR activates downstream components of a signaling cascade to maintain nucleotide pool balance, protect replication fork integrity, regulate activation of origins of replication, coordinate DNA repair, and implement cell cycle delay. This list of functions continues to expand as studies have revealed that Mec1/ATR modularly interacts with various protein molecules in response to different cellular cues. Among these newly assigned functions is the regulation of RNA metabolism during checkpoint activation and the coordination of replication–transcription conflicts. In this review, I will highlight some of these new functions of Mec1/ATR with a focus on the yeast model organism. View Full-Text
Keywords: Mec1/ATR; replication–transcription conflict; checkpoint; DNA damage response; stress response; R-loop Mec1/ATR; replication–transcription conflict; checkpoint; DNA damage response; stress response; R-loop

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Feng, W. Mec1/ATR, the Program Manager of Nucleic Acids Inc.. Genes 2017, 8, 10.

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