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乙烯在去黄化过程中对于子叶变绿和幼苗存活是至关重要的。

Ethylene is crucial for cotyledon greening and seedling survival during de-etiolation.

机构信息

The National Laboratory of Protein Engineering and Plant Genetic Engineering, College of Life Sciences, Peking University, Beijing, China.

出版信息

Plant Signal Behav. 2010 Jun;5(6):739-42. doi: 10.4161/psb.5.6.11698. Epub 2010 Jun 1.

Abstract

The most remarkable change of de-etiolation in seedling is chlorophyll synthesis and greening. This transition is achieved by photoreduction of dark-accumulated protochlorophyllide (Pchlide) in light. However, overaccumulation of Pchlide results in phototoxicity to plants, so appropriate accumulation and quick reduction of Pchlide are crucial for survival of seedlings during the transition from dark to light. We found that this vital process is tightly regulated by the plant gaseous hormone ethylene. Transgenic analysis using a promoter-GUS reporter system showed that the ethylene signaling was able to activate the expression of PORA (protochlorophyllide oxidoreductase A) gene in seedling cotyledons. We further found that application of ethylene rescued the greening defect of the flu mutant, which over-accumulated Pchlide in the dark. Additionally, genetic studies revealed that Ethylene Insensitive 3 (EIN3) and EIN3-like 1 (EIL1)regulate Pchlide accumulation and cotyledon greening largely independent of Phytochrome-Interacting Factor 1 (PIF1) but partly dependent on PIF3. Therefore, the ethylene signaling via EIN3/EIL1 presents a new pathway to constrain phototoxic Pchlide accumulation in darkness, and simultaneously facilitate Pchlide reduction to synthesize chlorophyll upon light exposure. Our results thus uncover an essential role of ethylene in protecting seedlings from photo-oxidative damage during the process of de-etiolation.

摘要

脱黄化过程中最显著的变化是叶绿素的合成和变绿。这种转变是通过在光下还原暗积累的原叶绿素(Pchlide)来实现的。然而,Pchlide 的过度积累会对植物造成光毒性,因此,在从黑暗到光明的过渡过程中,Pchlide 的适当积累和快速还原对于幼苗的存活至关重要。我们发现,这个重要过程受到植物气态激素乙烯的紧密调控。使用启动子-GUS 报告系统的转基因分析表明,乙烯信号能够激活幼苗子叶中 PORA(原叶绿素氧化还原酶 A)基因的表达。我们进一步发现,乙烯的应用挽救了 flu 突变体的变绿缺陷,该突变体在黑暗中过度积累 Pchlide。此外,遗传研究表明,Ethylene Insensitive 3 (EIN3) 和 EIN3-like 1 (EIL1)在很大程度上独立于 Phytochrome-Interacting Factor 1 (PIF1),但部分依赖于 PIF3,调控 Pchlide 积累和子叶变绿。因此,乙烯信号通过 EIN3/EIL1 提供了一种新的途径来限制黑暗中光毒性 Pchlide 的积累,同时促进 Pchlide 的还原以合成叶绿素。因此,我们的研究结果揭示了乙烯在脱黄化过程中保护幼苗免受光氧化损伤中的重要作用。

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