Deletion of the tobacco plastid psbA gene triggers an upregulation of the thylakoid-associated NAD(P)H dehydrogenase complex and the plastid terminal oxidase (PTOX)
Deletion of the tobacco plastid psbA gene triggers an upregulation of the thylakoid-associated NAD(P)H dehydrogenase complex and the plastid terminal oxidase (PTOX)
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DOI：
10.1046/j.1365-313x.2003.01842.x
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发表时间：
2003-09-01
期刊：
影响因子：
7.2
通讯作者：
Aro, EM
中科院分区：
文献类型：
--
作者：
Baena-González, E;Allahverdiyeva, Y;Aro, EM
我们构建了一个缺乏光系统II （PSII）复合物的烟草psbA基因缺失突变体。对类囊体膜的分析显示，在叶绿素基础上，野生型（WT）和DeltapsbA叶片的光系统I （PSI）、细胞色素b6f复合物和PSII光收集复合物（LHCII）天线蛋白的数量相当。然而，在突变体中缺乏PSII导致类囊体相关质体末端氧化酶（PTOX）和NAD(P)H脱氢酶（NDH）复合物的相对量增加了10倍以上。凝胶内NADH脱氢酶测量结果显示，在突变体类囊体中，Ndh多肽数量的增加伴随着Ndh活性的四倍以上增强。NADH还对DeltapsbA类囊体中P700（+）的再还原具有特异性刺激作用。总之，我们的研究结果表明，通过NDH复合物和可能的其他替代电子传递途径增强的电子流部分补偿了DeltapsbA突变体中PSII功能的丧失。由于WT和DeltapsbA植物的mRNA水平相当，可选择的电子传递途径（NDH复合物和PTOX）的上调显然是通过翻译或翻译后机制发生的。
We have constructed a tobacco psbA gene deletion mutant that is devoid of photosystem II (PSII) complex. Analysis of thylakoid membranes revealed comparable amounts, on a chlorophyll basis, of photosystem I (PSI), the cytochrome b6f complex and the PSII light-harvesting complex (LHCII) antenna proteins in wildtype (WT) and DeltapsbA leaves. Lack of PSII in the mutant, however, resulted in over 10-fold higher relative amounts of the thylakoid-associated plastid terminal oxidase (PTOX) and the NAD(P)H dehydrogenase (NDH) complex. Increased amounts of Ndh polypeptides were accompanied with a more than fourfold enhancement of NDH activity in the mutant thylakoids, as revealed by in-gel NADH dehydrogenase measurements. NADH also had a specific stimulating effect on P700(+) re-reduction in the DeltapsbA thylakoids. Altogether, our results suggest that enhancement of electron flow via the NDH complex and possibly other alternative electron transport routes partly compensates for the loss of PSII function in the DeltapsbA mutant. As mRNA levels were comparable in WT and DeltapsbA plants, upregulation of the alternative electron transport pathways (NDH complex and PTOX) occurs apparently by translational or post-translational mechanisms.