UVR2 ensures transgenerational genome stability under simulated natural UV-B in Arabidopsis thaliana

Ground levels of solar UV-B radiation induce DNA damage. Sessile phototrophic organisms such as vascular plants are recurrently exposed to sunlight and require UV-B photoreception, flavonols shielding, direct reversal of pyrimidine dimers and nucleotide excision repair for resistance against UV-B ra...

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Published in:Nature communications Vol. 7; no. 1; p. 13522
Main Authors: Willing, Eva-Maria, Piofczyk, Thomas, Albert, Andreas, Winkler, J. Barbro, Schneeberger, Korbinian, Pecinka, Ales
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 01-12-2016
Nature Publishing Group
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Summary:Ground levels of solar UV-B radiation induce DNA damage. Sessile phototrophic organisms such as vascular plants are recurrently exposed to sunlight and require UV-B photoreception, flavonols shielding, direct reversal of pyrimidine dimers and nucleotide excision repair for resistance against UV-B radiation. However, the frequency of UV-B-induced mutations is unknown in plants. Here we quantify the amount and types of mutations in the offspring of Arabidopsis thaliana wild-type and UV-B-hypersensitive mutants exposed to simulated natural UV-B over their entire life cycle. We show that reversal of pyrimidine dimers by UVR2 photolyase is the major mechanism required for sustaining plant genome stability across generations under UV-B. In addition to widespread somatic expression, germline-specific UVR2 activity occurs during late flower development, and is important for ensuring low mutation rates in male and female cell lineages. This allows plants to maintain genome integrity in the germline despite exposure to UV-B. As sessile organisms, plants are exposed to recurrent solar UV-B radiation that can induce DNA damage. Here, the authors characterize mutations that occur in Arabidopsis under light regimes simulating natural UV-B exposure and find that the UVR2 photolyase is the major component required to maintain genome stability.
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These authors contributed equally to this work
ISSN:2041-1723
DOI:10.1038/ncomms13522