Activation of cyclic electron flow by hydrogen peroxide in vivo
Activation of cyclic electron flow by hydrogen peroxide in vivo
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DOI：
10.1073/pnas.1418223112
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发表时间：
2015-04
期刊：
影响因子：
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通讯作者：
Deserah D. Strand;A. Livingston;Mio Satoh-Cruz;J. Froehlich;V. Maurino;D. Kramer
中科院分区：
文献类型：
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作者：
Deserah D. Strand;A. Livingston;Mio Satoh-Cruz;J. Froehlich;V. Maurino;D. Kramer
光系统I（CEF）周围的循环电子流对于平衡光合作用的能量收支至关重要，但其调节还不清楚。我们的研究结果提供了证据表明，过氧化氢，这是由于叶绿体氧化还原状态的不平衡产生的，作为一种信号剂，激活CEF在高等植物体内。光系统I周围的循环电子流（CEF）被认为是平衡光合作用的ATP/NADPH能量预算，需要对其速率进行精细调节。这种调节的机制尚不清楚。我们观察到，表现出组成型高CEF率的突变体也表现出H2 O2的产生升高。因此，我们测试的假设，CEF可以激活过氧化氢在体内。CEF强烈增加H2 O2的渗透或原位生产的叶绿体定位乙醇酸氧化酶，这意味着H2 O2可以激活CEF直接通过氧化还原调节的关键酶，或间接影响其他光合过程。暴露于H2 O2后，CEF出现的半衰期约为20分钟，这表明先前表达的CEF相关机制被激活。H2 O2依赖性CEF对抗霉素A或PGR 5的丢失不敏感，表明CEF增加可能不涉及PGR 5-PGRL 1相关通路。与此相反，没有观察到的突变体中缺乏的叶绿体NADPH：PQ还原酶（NDH）的CEF的上升，支持参与此复杂的CEF激活过氧化氢。我们认为H2 O2是高等植物中环境胁迫、代谢和CEF氧化还原调节之间缺失的一个环节。
Significance Cyclic electron flow around photosystem I (CEF) is critical for balancing the energy budget of photosynthesis, but its regulation is not well understood. Our results provide evidence that hydrogen peroxide, which is produced as a result of imbalances in chloroplast redox state, acts as a signaling agent to activate CEF in higher plants in vivo. Cyclic electron flow (CEF) around photosystem I is thought to balance the ATP/NADPH energy budget of photosynthesis, requiring that its rate be finely regulated. The mechanisms of this regulation are not well understood. We observed that mutants that exhibited constitutively high rates of CEF also showed elevated production of H2O2. We thus tested the hypothesis that CEF can be activated by H2O2 in vivo. CEF was strongly increased by H2O2 both by infiltration or in situ production by chloroplast-localized glycolate oxidase, implying that H2O2 can activate CEF either directly by redox modulation of key enzymes, or indirectly by affecting other photosynthetic processes. CEF appeared with a half time of about 20 min after exposure to H2O2, suggesting activation of previously expressed CEF-related machinery. H2O2-dependent CEF was not sensitive to antimycin A or loss of PGR5, indicating that increased CEF probably does not involve the PGR5-PGRL1 associated pathway. In contrast, the rise in CEF was not observed in a mutant deficient in the chloroplast NADPH:PQ reductase (NDH), supporting the involvement of this complex in CEF activated by H2O2. We propose that H2O2 is a missing link between environmental stress, metabolism, and redox regulation of CEF in higher plants.