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Photosynthetic electron transport regulates the expression of cytosolic ascorbate peroxidase genes in Arabidopsis during excess light stress.

机译:在过量的光胁迫下光合电子传递调节拟南芥中胞质抗坏血酸过氧化物酶基因的表达。

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摘要

Exposure of Arabidopsis plants that were maintained under low light (200 mumol of photons m-2 sec-1) to excess light (2000 mumol of photons m-2 sec-1) for 1 hr caused reversible photoinhibition of photosynthesis. Measurements of photosynthetic parameters and the use of electron transport inhibitors indicated that a novel signal transduction pathway was initiated at plastoquinone and regulated, at least in part, by the redox status of the plastoquinone pool. This signal, which preceded the photooxidative burst of hydrogen peroxide (H2O2) associated with photoinhibition of photosynthesis, resulted in a rapid increase (within 15 min) in mRNA levels of two cytosolic ascorbate peroxidase genes (APX1 and APX2). Treatment of leaves with exogenous reduced glutathione abolished this signal, suggesting that glutathione or the redox status of the glutathione pool has a regulatory impact on this signaling pathway. During recovery from photooxidative stress, transcripts for cytosolic glutathione reductase (GOR2) increased, emphasizing the role of glutathione in this stress.
机译:将维持在弱光下的拟南芥植物(200摩尔光子m-2 sec-1)暴露于过量光(2000摩尔的光子m-2 sec-1)1小时,引起光合作用的可逆光抑制。光合作用参数的测量和电子传递抑制剂的使用表明,新的信号转导途径始于质体醌,并至少部分受到质体醌池的氧化还原状态的调节。该信号先于与光合作用的光抑制相关的过氧化氢(H2O2)的光氧化爆发,导致两个胞质抗坏血酸过氧化物酶基因(APX1和APX2)的mRNA水平快速增加(在15分钟内)。用外源性还原型谷胱甘肽还原酶处理的叶片消除了该信号,表明谷胱甘肽或谷胱甘肽池的氧化还原状态对该信号通路具有调节作用。在从光氧化应激中恢复期间,胞质谷胱甘肽还原酶(GOR2)的转录本增加,强调了谷胱甘肽在这种应激中的作用。

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