Meeting Abstract
75.5 Monday, Jan. 6 09:00 DNA damage tolerance and photorepair of ultraviolet-C irradiated Austrofundulus limnaeus embryos: unique insight into annual killifish development WAGNER, J.T.*; PODRABSKY, J.E.; Portland State Univ.; Portland State Univ. josw@pdx.edu
Exposure of cells to ultraviolet radiation has long been known to cause DNA damage, with the most abundant form being cyclobutane pyrimidine dimers. If left unrepaired, these lesions can lead to mutations or cell death by apoptosis. Free-living eggs of oviparous aquatic organisms are particularly at risk of exposure to solar ultraviolet radiation, and must repair, tolerate, or block this radiation to complete normal development. Embryos of the annual killifish Austrofundulus limnaeus are capable of surviving long bouts of desiccation, anoxia, and extremes in salinity. Depending on environmental conditions, much of their life may be spent as an embryo in a state of metabolic and developmental arrest, also known as embryonic diapause. Here, I show that their stress tolerance extends to DNA damage caused by ultraviolet radiation. A. limnaeus embryos were irradiated with ultraviolet-C radiation (254 nm) with doses ranging from 0 J/m2 to 4,500 J/m2 at three distinct stages: before axis formation, during axis formation/somitogenesis, and during embryonic diapause. After exposure, embryos were allowed to recover under either full-spectrum lights or darkness and development was tracked. Irradiated embryos were also stained for DNA lesions and evidence of apoptosis. Interestingly, embryos at all three stages appear to be reliant on a photorepair mechanism to repair DNA lesions. In addition, diapausing embryos may be able to sustain massive DNA damage for several weeks without observable effects. These data suggest that while A. limnaeus embryos share DNA repair mechanisms with other aquatic organisms, these embryos may also possess unique strategies to cope with DNA damage that have not yet been described.
