Sirpiö Sari, Khrouchtchova Anastassia, Allahverdiyeva Yagut, Hansson Maria, Fristedt Rikard, Vener Alexander V, Scheller Henrik Vibe, Jensen Poul Erik, Haldrup Anna, Aro Eva-Mari
Department of Biology, Plant Physiology and Molecular Biology, University of Turku, FI-20014 Turku, Finland.
Plant J. 2008 Aug;55(4):639-51. doi: 10.1111/j.1365-313X.2008.03532.x. Epub 2008 Apr 24.
AtCYP38 is a thylakoid lumen protein comprising the immunophilin domain and the phosphatase inhibitor module. Here we show the association of AtCYP38 with the photosystem II (PSII) monomer complex and address its functional role using AtCYP38-deficient mutants. The dynamic greening process of etiolated leaves failed in the absence of AtCYP38, due to specific problems in the biogenesis of PSII complexes. Also the development of leaves under short-day conditions was severely disturbed. Detailed biophysical and biochemical analysis of mature AtCYP38-deficient plants from favorable growth conditions (long photoperiod) revealed: (i) intrinsic malfunction of PSII, which (ii) occurred on the donor side of PSII and (iii) was dependent on growing light intensity. AtCYP38 mutant plants also showed decreased accumulation of PSII, which was shown not to originate from impaired D1 synthesis or assembly of PSII monomers, dimers and supercomplexes as such but rather from the incorrect fine-tuning of the oxygen-evolving side of PSII. This, in turn, rendered PSII centers extremely susceptible to photoinhibition. AtCYP38 deficiency also drastically decreased the in vivo phosphorylation of PSII core proteins, probably related to the absence of the AtCYP38 phosphatase inhibitor domain. It is proposed that during PSII assembly AtCYP38 protein guides the proper folding of D1 (and CP43) into PSII, thereby enabling the correct assembly of the water-splitting Mn(4)-Ca cluster even with high turnover of PSII.
拟南芥CYP38是一种类囊体腔蛋白，包含亲环素结构域和磷酸酶抑制剂模块。在此我们展示了拟南芥CYP38与光系统II（PSII）单体复合物的关联，并利用拟南芥CYP38缺陷型突变体研究其功能作用。在缺乏拟南芥CYP38的情况下，黄化叶片的动态变绿过程失败，这是由于PSII复合物生物合成中存在特定问题。短日条件下叶片的发育也受到严重干扰。对来自有利生长条件（长光周期）的成熟拟南芥CYP38缺陷型植株进行详细的生物物理和生化分析发现：（i）PSII存在内在功能障碍，（ii）发生在PSII的供体侧，（iii）依赖于生长光强。拟南芥CYP38突变体植株还表现出PSII积累减少，这并非源于D1合成受损或PSII单体、二聚体和超级复合物本身的组装受损，而是源于PSII放氧侧的微调不正确。这反过来又使PSII中心极易受到光抑制。拟南芥CYP38缺陷还显著降低了PSII核心蛋白的体内磷酸化，这可能与拟南芥CYP38磷酸酶抑制剂结构域的缺失有关。有人提出，在PSII组装过程中，拟南芥CYP38蛋白引导D1（和CP43）正确折叠进入PSII，从而即使在PSII高周转率的情况下也能使水裂解Mn(4)-Ca簇正确组装。
