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Maintaining genome stability in the nervous system

Nature Neuroscience volume 16, pages 1523–1529 (2013)Cite this article

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Abstract

Active maintenance of genome stability is a prerequisite for the development and function of the nervous system. The high replication index during neurogenesis and the long life of mature neurons highlight the need for efficient cellular programs to safeguard genetic fidelity. Multiple DNA damage response pathways ensure that replication stress and other types of DNA lesions, such as oxidative damage, do not affect neural homeostasis. Numerous human neurologic syndromes result from defective DNA damage signaling and compromised genome integrity. These syndromes can involve different neuropathology, which highlights the diverse maintenance roles that are required for genome stability in the nervous system. Understanding how DNA damage signaling pathways promote neural development and preserve homeostasis is essential for understanding fundamental brain function.

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Figure 1: Different DNA repair pathways function during neural development.
Figure 2: DNA damage signaling in the nervous sytem involves ATM and ATR.
Figure 3: The cell cycle of cortical progenitors changes during development.
Figure 4: Defective DNA single-stranded break repair can result in syndrome with varied neuropathology.

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Acknowledgements

P.J.M. is supported by the US National Institutes of Health (NS-37956, CA-96832), a Cancer Center Support grant (P30 CA21765) and the American Lebanese and Syrian Associated Charities of St. Jude Children's Research Hospital.

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    Peter J McKinnon

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McKinnon, P. Maintaining genome stability in the nervous system. Nat Neurosci 16, 1523–1529 (2013). https://doi.org/10.1038/nn.3537

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