The light stress-induced protein ELIP2 is a regulator of chlorophyll synthesis in Arabidopsis thaliana.
The light stress-induced protein ELIP2 is a regulator of chlorophyll synthesis in Arabidopsis thaliana.
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DOI：
10.1111/j.1365-313x.2007.03090.x
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发表时间：
2007-06
期刊：
影响因子：
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通讯作者：
Tzvetelina Tzvetkova-Chevolleau;F. Franck;Ali E Alawady;L. Dall’Osto;F. Carrière;R. Bassi;B. Grimm
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文献类型：
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作者：
Tzvetelina Tzvetkova-Chevolleau;F. Franck;Ali E Alawady;L. Dall’Osto;F. Carrière;R. Bassi;B. Grimm
早期光诱导蛋白（ELIP）属于色素结合光捕获复合物的多基因家族。 ELIP 会短暂积累，并被认为对暴露在强光下的植物起到保护作用。拟南芥中 ELIP2 基因的组成型表达导致叶绿体色素含量显着减少，无论是在成熟叶子中还是在黄化幼苗变绿期间。叶绿素损失与类囊体膜中光系统数量的减少有关，但存在的光系统已完全组装并发挥功能。对叶绿素合成途径的详细分析表明，ELIP2 积累下调了两个重要调节步骤的水平和活性：5-氨基乙酰丙酸合成和镁原卟啉 IX (Mg-Proto IX) 螯合酶活性。谷氨酰 tRNA 还原酶和镁螯合酶亚基 CHLH 和 CHLI 的含量因 ELIP2 积累而降低。相反，亚铁螯合酶活性不受影响，并且对血红素合成的抑制为零或非常温和。由于 5-氨基乙酰丙酸的代谢流减少，各种叶绿素前体（从原卟啉 IX 到原叶绿素内酯）的稳态水平在 ELIP2 过表达细胞中大幅降低。综上所述，我们的结果表明 ELIP 的生理功能可能与类囊体中叶绿素浓度的调节有关。这似乎是通过抑制四吡咯的初始前体 5-氨基乙酰丙酸的整个叶绿素生物合成途径而发生的。我们建议 ELIP 作为叶绿素传感器，调节叶绿素合成，防止游离叶绿素积累，从而防止光氧化应激。
The early light-induced proteins (ELIPs) belong to the multigenic family of pigment-binding light-harvesting complexes. ELIPs accumulate transiently and are believed to play a protective role in plants exposed to high levels of light. Constitutive expression of the ELIP2 gene in Arabidopsis resulted in a marked reduction of the pigment content of the chloroplasts, both in mature leaves and during greening of etiolated seedlings. The chlorophyll loss was associated with a decrease in the number of photosystems in the thylakoid membranes, but the photosystems present were fully assembled and functional. A detailed analysis of the chlorophyll-synthesizing pathway indicated that ELIP2 accumulation downregulated the level and activity of two important regulatory steps: 5-aminolevulinate synthesis and Mg-protoporphyrin IX (Mg-Proto IX) chelatase activity. The contents of glutamyl tRNA reductase and Mg chelatase subunits CHLH and CHLI were lowered in response to ELIP2 accumulation. In contrast, ferrochelatase activity was not affected and the inhibition of Heme synthesis was null or very moderate. As a result of reduced metabolic flow from 5-aminolevulinic acid, the steady state levels of various chlorophyll precursors (from protoporphyrin IX to protochlorophyllide) were strongly reduced in the ELIP2 overexpressors. Taken together, our results indicate that the physiological function of ELIPs could be related to the regulation of chlorophyll concentration in thylakoids. This seems to occur through an inhibition of the entire chlorophyll biosynthesis pathway from the initial precursor of tetrapyrroles, 5-aminolevulinic acid. We suggest that ELIPs work as chlorophyll sensors that modulate chlorophyll synthesis to prevent accumulation of free chlorophyll, and hence prevent photooxidative stress.