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首页> 外文期刊>Global change biology >Cooler temperatures slow the repair of DNA damage in tadpoles exposed to ultraviolet radiation: Implications for amphibian declines at high altitude
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Cooler temperatures slow the repair of DNA damage in tadpoles exposed to ultraviolet radiation: Implications for amphibian declines at high altitude

机译:冷却器温度减缓暴露于紫外线辐射的蝌蚪的DNA损伤的修复:对两栖动物的影响在高海拔地区下降

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摘要

Ultraviolet B radiation (UVBR) damages the DNA of exposed cells, causing dimers to form between adjacent pyrimidine nucleotides. These dimers block DNA replication, causing mutations and apoptosis. Most organisms utilize biochemical or biophysical DNA repair strategies to restore DNA structure; however, as with most biological reactions, these processes are likely to be thermally sensitive. Tadpoles exposed to elevated UVBR at low environmental temperatures have significantly higher rates of mortality and developmental deformities compared with tadpoles exposed to the same levels of UVBR at higher environmental temperatures. We hypothesized that low environmental temperatures impair the primary enzymatic (photolyase) DNA repair pathway in amphibians, leading to the accumulation of DNA damage. To test this hypothesis, we compared DNA repair rates and photolyase gene expression patterns in Limnodynastes peronii. Tadpoles were acutely exposed to UVBR for 1 hr at either 20 or 30 degrees C, and we measured DNA damage and photolyase expression levels at intervals following this exposure. Temperature had a significant effect on the rate of DNA repair, with repair at 30 degrees C occurring twice as fast as repair at 20 degrees C. Photolyase gene expression (6-4 PP and CPD) was significantly upregulated by UVBR exposure, with expression levels increasing within 6 hr of UVBR exposure. CPD expression levels were not significantly affected by temperature, but 6-4 PP expression was significantly higher in tadpoles in the 30 degrees C treatment within 12 hr of UVBR exposure. These data support the hypothesis that DNA repair rates are thermally sensitive in tadpoles and may explain why enigmatic amphibian declines are higher in montane regions where UVBR levels are naturally elevated and environmental temperatures are lower.
机译:紫外线B辐射(UVBR)损坏暴露细胞的DNA,导致在相邻嘧啶核苷酸之间形成二聚体。这些二聚体阻断DNA复制,引起突变和细胞凋亡。大多数生物利用生物化学或生物物理DNA修复策略来恢复DNA结构;然而,与大多数生物反应一样,这些过程可能是热敏的。与在较高环境温度下暴露于相同水平的UVBR暴露于相同水平的蝌蚪相比,在低环境温度下暴露于升高的UVBR的蝌蚪具有明显更高的死亡率和发育畸形。我们假设低环境温度损害两栖动物中的初级酶(光学酶)DNA修复途径,导致DNA损伤的积累。为了测试这一假设,我们将DNA修复率和光聚酶基因表达模式与Limnodydasts Peronii进行了比较。在20或30摄氏度下,蝌蚪急性地暴露于UVBR 1小时,并且在这种暴露后,我们以间隔测量DNA损伤和光降解酶表达水平。温度对DNA修复的速率具有显着影响,在30摄氏度下修复两次,在20℃的修复时发生两倍。通过UVBR暴露显着上调光降解酶基因表达(6-4pp和CPD),具有表达水平在UVBR暴露的6小时内增加。 CPD表达水平没有受到温度的显着影响,但在uvBR暴露的12小时内的30摄氏度处理中,蝌蚪在蝌蚪中显着较高。这些数据支持假设,即DNA修复率在蝌蚪中热敏感,并且可以解释为什么蒙太烷区域的神经膜层下降较高,其中UVBR水平自然升高,环境温度较低。

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