Molecular mechanisms of divergent adaptation to a variable environmental stressor among neighboring Daphnia populations

Background/Question/Methods

Understanding the mechanisms by which populations of organisms have adapted to environmental stressors in the recent past is critical to predicting responses to changing environments in the future. Of particular interest is phenotypic divergence among closely related populations that experience differing intensities of a common environmental stressor in otherwise similar habitats. When phenotypic differences between such populations can be traced to the molecular level, we can begin to understand the ways in which genes and gene expression can (and cannot) respond to environmental change. We have previously documented differences in tolerance of ultraviolet radiation (UVR) among neighboring populations of the freshwater crustacean Daphnia melanica inhabiting subalpine ponds that differ widely in transparency to UVR. Daphnia from ponds more transparent to UVR are more tolerant of UVR in laboratory trials, but the mechanism for this divergence was previously unknown.

Results/Conclusions

Here we present the results of a multifaceted investigation of the possible mechanisms to explain differences in UVR tolerance among these populations. We rule out the existence of photoprotective pigmentation by demonstrating the absence of both melanin and mycosporine-like amino acids (MAAs) in our study populations. Behavioral avoidance of UVR is assumed but is not sufficient to explain the divergence in UVR tolerance as measured in laboratory trials that restricted this ability. Hence we focus on a third mechanism, the capacity for repair of UVR-induced DNA damage. We demonstrate that the survival advantage of lineages more tolerant of UVR is not present in the absence of the visible wavelengths of light known to power the photoenzymatic repair process, a critical mechanism of UVR tolerance in freshwater zooplankton. We show that UVR-induced DNA damage, as measured by ELISA, is more efficient in lineages more tolerant of UVR. In addition, we explore expression of the gene photorepair, which is responsible for performing photoenzymatic DNA repair. We find that lineages differ greatly in their expression of photorepair, and infer that this mechanism, mediated by expression of a single gene, is responsible for adaptive divergence among natural populations inhabiting differing UVR environments.