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一氧化氮抑制蓝藻集胞藻PCC 6803中的光系统II和NDH-1。

Nitric oxide represses photosystem II and NDH-1 in the cyanobacterium Synechocystis sp. PCC 6803.

作者信息

Solymosi Daniel, Shevela Dmitry, Allahverdiyeva Yagut

机构信息

Molecular Plant Biology, Department of Life Technologies, University of Turku, Turku, FI 20014, Finland.

Chemical Biological Centre, Department of Chemistry, Umeå University, 90187 Umeå, Sweden.

出版信息

Biochim Biophys Acta Bioenerg. 2022 Jan 1;1863(1):148507. doi: 10.1016/j.bbabio.2021.148507. Epub 2021 Oct 30.

DOI:10.1016/j.bbabio.2021.148507
PMID:34728155
Abstract

Photosynthetic electron transfer comprises a series of light-induced redox reactions catalysed by multiprotein machinery in the thylakoid. These protein complexes possess cofactors susceptible to redox modifications by reactive small molecules. The gaseous radical nitric oxide (NO), a key signalling molecule in green algae and plants, has earlier been shown to bind to Photosystem (PS) II and obstruct electron transfer in plants. The effects of NO on cyanobacterial bioenergetics however, have long remained obscure. In this study, we exposed the model cyanobacterium Synechocystis sp. PCC 6803 to NO under anoxic conditions and followed changes in whole-cell fluorescence and oxidoreduction of P700 in vivo. Our results demonstrate that NO blocks photosynthetic electron transfer in cells by repressing PSII, PSI, and likely the NDH dehydrogenase-like complex 1 (NDH-1). We propose that iron‑sulfur clusters of NDH-1 complex may be affected by NO to such an extent that ferredoxin-derived electron injection to the plastoquinone pool, and thus cyclic electron transfer, may be inhibited. These findings reveal the profound effects of NO on Synechocystis cells and demonstrate the importance of controlled NO homeostasis in cyanobacteria.

摘要

光合电子传递包括一系列由类囊体中的多蛋白机制催化的光诱导氧化还原反应。这些蛋白质复合物含有易受活性小分子氧化还原修饰影响的辅因子。气态自由基一氧化氮(NO)是绿藻和植物中的关键信号分子,此前已被证明可与光系统(PS)II结合并阻碍植物中的电子传递。然而,长期以来,NO对蓝藻生物能量学的影响一直不清楚。在本研究中,我们在缺氧条件下将模式蓝藻集胞藻PCC 6803暴露于NO中,并跟踪体内全细胞荧光和P700的氧化还原变化。我们的结果表明,NO通过抑制PSII、PSI以及可能的类NDH脱氢酶复合物1(NDH-1)来阻断细胞中的光合电子传递。我们提出,NDH-1复合物的铁硫簇可能受到NO的影响,以至于来自铁氧化还原蛋白的电子注入到质体醌库中,从而抑制循环电子传递。这些发现揭示了NO对集胞藻细胞的深远影响,并证明了控制蓝藻中NO稳态的重要性。

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