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首页> 外文期刊>Journal of Experimental Botany >Mutation of Arabidopsis HY1 causes UV-C hypersensitivity by impairing carotenoid and flavonoid biosynthesis and the down-regulation of antioxidant defence
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Mutation of Arabidopsis HY1 causes UV-C hypersensitivity by impairing carotenoid and flavonoid biosynthesis and the down-regulation of antioxidant defence

机译：拟南芥HY1的突变通过削弱类胡萝卜素和类黄酮的生物合成以及抗氧化剂防御的下调而引起UV-C超敏反应

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Previous pharmacological results confirmed that haem oxygenase-1 (HO-1) is involved in protection of cells against ultraviolet (UV)-induced oxidative damage in soybean [Glycine max (L.) Merr.] seedlings, but there remains a lack of genetic evidence. In this study, the link between Arabidopsis thaliana HO-1 (HY1) and UV-C tolerance was investigated at the genetic and molecular levels. The maximum inducible expression of HY1 in wild-type Arabidopsis was observed following UV-C irradiation. UV-C sensitivity was not observed in ho2, ho3, and ho4 single and double mutants. However, the HY1 mutant exhibited UV-C hypersensitivity, consistent with the observed decreases in chlorophyll content, and carotenoid and flavonoid metabolism, as well as the down-regulation of antioxidant defences, thereby resulting in severe oxidative damage. The addition of the carbon monoxide donor carbon monoxide-releasing molecule-2 (CORM-2), in particular, and bilirubin (BR), two catalytic by-products of HY1, partially rescued the UV-C hypersensitivity, and other responses appeared in the hy1 mutant. Transcription factors involved in the synthesis of flavonoid or UV responses were induced by UV-C, but reduced in the hy1 mutant. Overall, the findings showed that mutation of HY1 triggered UV-C hypersensitivity, by impairing carotenoid and flavonoid synthesis and antioxidant defences.
机译：先前的药理结果证实，血红素加氧酶-1（HO-1）参与保护细胞免受大豆（Glycine max（L.）Merr。）幼苗中紫外线（UV）诱导的氧化损伤的影响，但仍然缺乏遗传证据。在这项研究中，在基因和分子水平上研究了拟南芥HO-1（HY1）与UV-C耐受性之间的联系。 UV-C照射后观察到HY1在野生型拟南芥中的最大诱导表达。在ho2，ho3和ho4单突变体和双突变体中未观察到UV-C敏感性。但是，HY1突变体表现出UV-C超敏性，与观察到的叶绿素含量下降，类胡萝卜素和类黄酮代谢以及抗氧化剂防御的下调一致，从而导致严重的氧化损伤。特别是添加一氧化碳供体一氧化碳释放分子2（CORM-2）和胆红素（BR），这是HY1的两种催化副产物，部分缓解了UV-C超敏反应，并且在hy1突变体。 UV-C诱导了类黄酮合成或UV反应合成的转录因子，但在hy1突变体中却降低了。总体而言，研究结果表明，HY1的突变通过削弱类胡萝卜素和类黄酮的合成以及抗氧化防御能力而引发UV-C超敏反应。

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