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The post translational modification of key regulators of ATR signaling in DNA replication

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Abstract

DNA replication is one of the most critical psychological process, which mainly consists of three steps: initiation, elongation, and termination. Precise regulation through all stages of DNA replication is essential for maintaining genome integrity in proliferating cells. During each cell cycle, the complete genetic information existing in the DNA needs to be duplicated and passed on to the daughter cells. The DNA replication machinery is confronted with many challenges and stresses owing to endogenous and exogenous facts that could harm the faithful duplication of the DNA. The abnormality of DNA replication could cause genomic instability and tumorigenesis. ATR is a master regulator of cells in response to DNA replication stress to safeguard genomic stability and prevent tumorigenesis. In the past years, the key functions of post-translational modification (PTM) in ATR signaling transduction has been explored. ATR signaling is complicatedly and tightly regulated by multiple PTMs, such as phosphorylation, acetylation, ubiquitination, SUMOylation and so on. Here, we summarize how the ATR signaling pathway is tightly regulated by PTM. Furthermore, we describe the critical roles of ATR signaling in DNA replication and safeguarding genomic stability. In the past years, the key functions of post-translational modification (PTM) in DNA replication has been explored. These findings benefit for us better understand the complicated mechanism of DNA replication signaling pathway.

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Acknowledgements

We gratefully acknowledge funding from National Natural Science Foundation(32070713 to J.Y., 82002985 to Y.P.C., 32090032 to J.Y.), Shanghai Pujiang program(2020PJD070 to Y.P.C.) and China Postdoctoral Science Foundation (2020M681384 to Y.P.C.).

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Correspondence to Jian Yuan.

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The authors declare that they have no competing interests.

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Chen, Y., Yuan, J. The post translational modification of key regulators of ATR signaling in DNA replication. GENOME INSTAB. DIS. 2, 92–101 (2021). https://doi.org/10.1007/s42764-021-00036-z

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  • DOI: https://doi.org/10.1007/s42764-021-00036-z

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