Extreme tolerance and developmental buffering of UV‐C induced DNA damage in embryos of the annual killifish Austrofundulus limnaeus

• DOI: 10.1002/jez.1890
• Publication Date: 2014-11-11T16:38:01Z
• Authors: Josiah T. Wagner; Jason E. Podrabsky
• Keywords: Killifish; Pyrimidine dimer; Photolyase

Free-living aquatic embryos are often at risk of exposure to ultraviolet radiation (UV-R). Successful completion embryonic development depends on efficient removal DNA lesions, and thus many have mechanisms reverse lesions induced by UV-R. However, little is known how that able enter dormancy may respond UV-R subsequent damage. Embryos the annual killifish Austrofundulus limnaeus unique among vertebrates because their normal includes (1) a complete dispersion blastomeres prior formation definitive axis, (2) entry into state metabolic depression developmental arrest termed diapause. Here, we show developing diapausing A. exceptional tolerance UV-C can successfully after receiving substantial doses UV-C, especially if allowed recover in full-spectrum light. Recovery light permits most common type lesion UV-R: cyclobutane pyrimidine dimers. Interestingly, whole-mount embryo TUNEL assays suggest apoptosis not be major contributor cell death irradiated during dispersion/reaggregation or We also observed mortality significantly delayed several weeks dark. These atypical responses damage due life history provide insight repair recognition dormancy.