缺铁对大豆叶片光合作用和光合系统 II 功能的影响

植物生理与分子生物学学报 Pub Date : 2007-02-01
Chuang-Dao Jiang, Hui-Yuan Gao, Qi Zou, Lei Shi
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引用次数: 0

摘要

研究了大豆植株的气体交换和叶绿素 a 荧光,以探讨缺铁对体内光合作用和光系统 II 功能的影响。缺铁导致净光合作用(Pn)急剧下降。与正常植株相比,缺铁植株中 PSII 光化学的最大量子产率(psipo)仅略有降低;而被捕获的激子将电子转移到比 QA- 更远的电子传递链中的效率(Psio)和超出 QA 的电子传递量子产率(psiEo)则显著降低。缺铁还导致 K 阶相对可变荧光(VK)明显增强。在光照下,缺铁植物开放的 PSII 反应中心的激发能量捕获效率(Fv'/Fm')、PSII 电子传递量子产率(PhiPSII)和光化学淬灭系数(qP)明显降低,但非光化学淬灭(NPQ)明显升高。此外,缺铁植物在光照后叶绿素荧光的瞬时增加明显增强。根据这些数据,我们认为缺铁导致 PSII 复合物的供体侧和受体侧均受损;缺铁大豆植株 PSI 周围的循环电子传递可能在诱导激发能量耗散和满足额外 ATP 需求以补偿磷酸化能力损失方面发挥了重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of iron deficiency on photosynthesis and photosystem II function in soybean leaf.

Gas exchange and chlorophyll a fluorescence in soybean plants were investigated to explore the effects of iron deficiency on photosynthesis and photosystem II function in vivo. Iron deficiency induced a drastic decrease in net photosynthesis (Pn). Compared with normal plants, the maximal quantum yield of PSII photochemistry (psipo) in iron-deficient plants was only slightly lower; whereas, the efficiency with which a trapped exciton can move an electron into the electron transport chain further than QA-(Psio) and quantum yield of electron transport beyond QA (psiEo) were significantly depressed. Iron deficiency also caused a clear enhancement of the relative variable fluorescence at K step (VK). When exposed to light, iron-deficient plants had considerably lower efficiency of excitation energy capture by open PSII reaction centers (Fv'/Fm'), quantum yield of PSII electron transport (PhiPSII), and photochemical quenching coefficient (qP), but markedly higher non-photochemical quenching (NPQ). In addition, post-illumination transient increase in chlorophyll fluorescence was clearly enhanced in iron-deficient plants. Basing on these data, we suggest that both the donor and the acceptor sides of PSII complex were damaged by iron deficiency; cyclic electron transport around PSI in iron-deficient soybean plants might play an important role in inducing the excitation energy dissipation and meeting the demand for extra ATP as a compensation for the loss of phosphorylation capability.

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