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拟南芥衰老基生叶中光合机构的损伤:反应中心 II 失活的一种可能机制。

Damage of photosynthetic apparatus in the senescing basal leaf of Arabidopsis thaliana: a plausible mechanism of inactivation of reaction center II.

机构信息

School of Life Sciences, Sambalpur University, Jyoti Vihar, 768019, Odisha, India.

出版信息

Plant Physiol Biochem. 2013 Jan;62:116-21. doi: 10.1016/j.plaphy.2012.10.018. Epub 2012 Nov 14.

DOI:10.1016/j.plaphy.2012.10.018
PMID:23220185
Abstract

Significant decline in oxygen evolution and DCPIP photoreduction and a marginal restoration of the later with DPC as an electron donor suggest the inactivation of reaction center of photosystem II. The declines in the height of thermoluminescence bands support the view and the damage of reaction center II could be central to the senescence process in Arabidopsis leaves. The enhancement in the number of reduced quinones, signifying a loss in redox homeostasis in the electron transport chain between photosystem II and I leads to the creation of an energy imbalance. The view is supported by the decline in actual quantum yield of photosystem II in the light adapted state and maximum quantum yield of primary photochemistry in the dark adapted state of chlorophyll fluorescence. An increase in chlorophyll a fluorescence polarization and decline in carotenoid to chlorophyll energy transfer efficiency suggest the perturbation in thylakoid structure. A plausible mechanism illustrating the senescence mediated inactivation of oxygen evolving complex has been proposed.

摘要

氧释放和 DCPIP 光还原显著下降,而 DPC 作为电子供体则略有恢复,这表明光合作用系统 II 的反应中心失活。热致发光带高度下降支持了这一观点,并且反应中心 II 的损伤可能是拟南芥叶片衰老过程的核心。还原醌数量的增加表明,在光合作用系统 II 和 I 之间的电子传递链中,氧化还原平衡丧失,导致能量失衡。这一观点得到了以下事实的支持:在光适应状态下,光合作用系统 II 的实际量子产率下降,以及在暗适应状态下叶绿素荧光的初级光化学最大量子产率下降。叶绿素 a 荧光偏振度增加和类胡萝卜素向叶绿素能量传递效率下降表明类囊体结构受到干扰。已经提出了一种说明衰老介导的氧释放复合物失活的可能机制。

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引用本文的文献

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Loss in photosynthesis during senescence is accompanied by an increase in the activity of β-galactosidase in leaves of Arabidopsis thaliana: modulation of the enzyme activity by water stress.拟南芥叶片衰老过程中光合作用的丧失伴随着β-半乳糖苷酶活性的增加:水分胁迫对该酶活性的调节。
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