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光系统 I 中铁硫簇的光损伤诱导非光化学能量耗散。

Photodamage of iron-sulphur clusters in photosystem I induces non-photochemical energy dissipation.

机构信息

Department of Biochemistry, Molecular Plant Biology, University of Turku, FI-20014 Turku, Finland.

Molecular Biomimetics, Department of Chemistry-Ångström Laboratory, Uppsala University, Box 523, SE-75120 Uppsala, Sweden.

出版信息

Nat Plants. 2016 Mar 21;2:16035. doi: 10.1038/nplants.2016.35.

Abstract

Photosystem I (PSI) uses light energy and electrons supplied by photosystem II (PSII) to reduce NADP(+) to NADPH. PSI is very tolerant of excess light but extremely sensitive to excess electrons from PSII. It has been assumed that PSI is protected from photoinhibition by strict control of the intersystem electron transfer chain (ETC). Here we demonstrate that the iron-sulphur (FeS) clusters of PSI are more sensitive to high light stress than previously anticipated, but PSI with damaged FeS clusters still functions as a non-photochemical photoprotective energy quencher (PSI-NPQ). Upon photoinhibition of PSI, the highly reduced ETC further triggers thylakoid phosphorylation-based mechanisms that increase energy flow towards PSI. It is concluded that the sensitivity of FeS clusters provides an additional photoprotective mechanism that is able to downregulate PSII, based on PSI quenching and protein phosphorylation.

摘要

光系统 I(PSI)利用来自光系统 II(PSII)的光能和电子将 NADP(+)还原为 NADPH。PSI 对过量的光具有很强的耐受性,但对来自 PSII 的过量电子非常敏感。人们一直认为,PSI 通过严格控制电子传递链(ETC)来防止光抑制。在这里,我们证明 PSI 的铁硫(FeS)簇比之前预期的对高光胁迫更为敏感,但 PSI 的 FeS 簇受损后仍然可以作为非光化学的光保护能量猝灭剂(PSI-NPQ)发挥作用。在 PSI 光抑制后,高度还原的 ETC 进一步触发类囊体磷酸化机制,增加能量流向 PSI。结论是,FeS 簇的敏感性提供了一种额外的光保护机制,能够基于 PSI 猝灭和蛋白磷酸化来下调 PSII。

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