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Hydrogen peroxide nitric oxide and UV RESISTANCE LOCUS8 interact to mediate UV-B-induced anthocyanin biosynthesis in radish sprouts

机译:过氧化氢一氧化氮和抗UV LOCUS8相互作用介导萝卜芽中UV-B诱导的花色苷生物合成

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摘要

The cross talk among hydrogen peroxide (H2O2), nitric oxide (NO) and UV RESISTANCE LOCUS8 (UVR8) in UV-B-induced anthocyanin accumulation in the hypocotyls of radish sprouts was investigated. The results showed that UV-B irradiation significantly increased the anthocyanin accumulation and the expression of UVR8, and a similar trend appeared in radish sprouts subjected to cadmium, chilling and salt stresses regardless of light source. However, these responses disappeared under dark exposure. These results suggest that abiotic stress-induced anthocyanin accumulation and UVR8 expression were light-dependent. Moreover, abiotic stresses all enhanced the production of H2O2 and exogenous H2O2 addition significantly increased the anthocyanin concentration and UVR8 transcription, while these increases were severely inhibited by addition of dimethylthiourea (DMTU, a chemical trap for H2O2). It seems to suggest that H2O2 played an important role in the anthocyanin biosynthesis. Furthermore, addition of 0.5 mM sodium nitroprusside (SNP, a NO-releasing compound) substantially induced the anthocyanin accumulation, and H2O2-induced anthocyanin accumulation and UVR8 expression were significantly suppressed by co-treatment with 2-phenyl-4,4,5,5-tetramethylimidazoline-3-oxide-1-oxyl (PTIO, a NO scavenger), which was parallel with the expression of anthocyanin biosynthesis-related transcription factors and structural genes. All these results demonstrate that both H2O2 and NO are involved in UV-B-induced anthocyanin accumulation, and there is a crosstalk between them as well as a classical UVR8 pathway.
机译:研究了过氧化氢(H2O2),一氧化氮(NO)和紫外线抵抗LOCUS8(UVR8)之间的相互作用,这些相互作用是由紫外线-B诱导的萝卜芽菜下胚轴花青素积累的。结果表明,UV-B辐射显着增加了花青素的积累和UVR8的表达,并且在受到镉,寒冷和盐胁迫的萝卜芽中,无论使用哪种光源,其趋势都相似。然而,这些反应在黑暗暴露下消失了。这些结果表明非生物胁迫诱导的花色苷积累和UVR8表达是光依赖性的。此外,非生物胁迫均增加了H2O2的产生,外源H2O2的添加显着增加了花色苷浓度和UVR8转录,而这些增加却因添加二甲基硫脲(DMTU,H2O2的化学陷阱)而受到严重抑制。似乎表明H2O2在花色苷的生物合成中起着重要作用。此外,添加0.5μmM的硝普钠(SNP,一种NO释放化合物)基本上诱导了花色苷的积累,并且通过与2-苯基-4,4,5共同处理显着抑制了H2O2诱导的花色苷的积累和UVR8的表达, 5-四甲基咪唑啉-3-氧化物-1-氧基(PTIO,NO清除剂),与花色苷生物合成相关的转录因子和结构基因的表达平行。所有这些结果表明,H2O2和NO都参与UV-B诱导的花色苷积累,并且在它们之间以及经典的UVR8途径之间存在串扰。

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