Data from: Divergence in DNA photorepair efficiency among genotypes from contrasting UV radiation environments in nature
Miner, Brooks E., Cornell University
Kulling, Paige M., Cornell University
Beer, Karlyn D., University of Washington, Institute for Systems Biology
Kerr, Benjamin, University of Washington
Published Nov 05, 2015 on Dryad.
Cite this dataset
Miner, Brooks E.; Kulling, Paige M.; Beer, Karlyn D.; Kerr, Benjamin (2015). Data from: Divergence in DNA photorepair efficiency among genotypes from contrasting UV radiation environments in nature [Dataset]. Dryad. https://doi.org/10.5061/dryad.k78f6
Populations of organisms routinely face abiotic selection pressures, and a central goal of evolutionary biology is to understand the mechanistic underpinnings of adaptive phenotypes. Ultraviolet radiation (UVR) is one of earth’s most pervasive environmental stressors, potentially damaging DNA in any organism exposed to solar radiation. We explored mechanisms underlying differential survival following UVR exposure in genotypes of the water flea Daphnia melanica derived from natural ponds of differing in UVR intensity. The UVR tolerance of a D. melanica genotype from a high-UVR habitat depended on the presence of visible and UV-A light wavelengths necessary for photoenzymatic repair of DNA damage, a repair pathway widely shared across the tree of life. We then measured the acquisition and repair of cyclobutane pyrimidine dimers, the primary form of UVR-caused DNA damage, in D. melanica DNA following experimental UVR exposure. We demonstrate that genotypes from high-UVR habitats repair DNA damage faster than genotypes from low-UVR habitats in the presence of visible and UV-A radiation necessary for photoenzymatic repair, but not in dark treatments. Because differences in repair rate only occurred in the presence of visible and UV-A radiation, we conclude that differing rates of DNA repair, and therefore differential UVR tolerance, are a consequence of variation in photoenzymatic repair efficiency. We then rule out a simple gene expression hypothesis for the molecular basis of differing repair efficiency, as expression of the CPD photolyase gene photorepair did not differ among D. melanica lineages, both in the presence and absence of UVR.
Source pond GPS coordinates
Data shown in Fig. 1. Number of starting animals and number of surviving animals after UV-B exposure and subsequent exposure to photorepair radiation (light) or no radiation (dark).
DNA damage data
Data shown in Fig 2A & 2B, with statistical results shown in Table 1. Data are absorbance values from ELISA for cyclobutane pyrimidine dimers (CPDs) in DNA.
qPCR data for photorepair gene
Raw Ct (cycle threshold) values from quantitative PCR, used to calculate relative expression values for photorepair gene shown in Fig. 3. Loci abbreviations are as follows: phr = photorepair, EF1A = elongation factor 1-alpha (reference gene), ATUB = alpha-tubulin (reference gene), G3PD = glyceraldegyde-3-phosphate dehydrogenase (reference gene)
DNA damage data (dark treatment)
Data shown in Fig 2C. Data are absorbance values from ELISA for cyclobutane pyrimidine dimers (CPDs) in DNA.
Carotenoid data shown in figure in Supporting Information.