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The origin of oxidized guanine resolves the puzzle of oxidation-induced telomere-length alterations

Nature Structural & Molecular Biology volume 23, pages 1070–1071 (2016)Cite this article

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Although oxidative stress has long been considered to be a major factor contributing to telomere shortening, recent work has established that oxidative stress and DNA damage are linked to telomere lengthening. Now, Opresko and colleagues resolve this apparent discrepancy by showing that differential modulation of telomerase activity depends on the origin of a common oxidative guanine lesion.

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Figure 1: Origin and consequences of oxidative DNA base damage within telomeres.

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Acknowledgements

This work was supported by the Intramural Research Program of the National Institutes of Health, National Institute on Aging.

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Authors and Affiliations

  1. Jaya Sarkar and Yie Liu are at the Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA.,

    Jaya Sarkar & Yie Liu

  2. Jaya Sarkar is presently at the Department of Biophysics, Johns Hopkins University, Baltimore, Maryland, USA.,

    Jaya Sarkar

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  1. Jaya Sarkar
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  2. Yie Liu
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Correspondence to Yie Liu.

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Sarkar, J., Liu, Y. The origin of oxidized guanine resolves the puzzle of oxidation-induced telomere-length alterations. Nat Struct Mol Biol 23, 1070–1071 (2016). https://doi.org/10.1038/nsmb.3332

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