Inactivation of the STT7 gene protects PsaF-deficient Chlamydomonas reinhardtii cells from oxidative stress under high light
Inactivation of the STT7 gene protects PsaF-deficient Chlamydomonas reinhardtii cells from oxidative stress under high light
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DOI：
10.1111/j.1399-3054.2010.01421.x
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发表时间：
2011-02-01
影响因子：
6.4
通讯作者：
Wilson, Kenneth E.
中科院分区：
文献类型：
--
作者：
Berry, Lindsay L.;Brzezowski, Pawel;Wilson, Kenneth E.
光系统I（PSI）利用光能激发电子以还原NADP+，并且像光系统II一样，它对过量的光敏感。当PSI被激发并且不能被电子传递链还原时，特殊的叶绿素分子对P700+将从邻近来源获取电子，导致细胞损伤。一个衣原体reinhardtii突变体，这是有缺陷的PSI的PsaF亚基的生产，提供了一个理想的平台，研究过程中涉及的保护PSI从过量的光。该菌株在暴露于强光（HL）后由于光氧化损伤而死亡。我们使用了第二个网站的抑制筛选，以确定参与保护PsaF缺陷PSI从过量的光基因。在这样做的过程中，我们证明了LHCII磷酸化和状态转换过程所需的STT 7蛋白的缺乏抑制了psaF HL-致死表型。的叶绿素荧光测量的基础上，psaF突变体有一个更减少plastoquinone池在一个给定的光合光子通量密度比野生型细胞。在这些条件下，状态转换过程将变得活跃，导致磷酸化LHCII蛋白转移到PSI，进一步增加PSI的激发。然而，在psaF stt 7双突变体中，LHCII蛋白不会转移到PSI，因此PSI激发的水平将保持较低。这项研究提供了明确的遗传证据，HL致死表型的psaF突变体是因为PSI过度。
Photosystem I (PSI) utilizes light energy to excite electrons for the reduction of NADP+, and like photosystem II, it is sensitive to excess light. When PSI is excited and unable to be reduced by the electron transport chain, the special pair of chlorophyll molecules, P700+, will take electrons from neighboring sources leading to cellular damage. A Chlamydomonas reinhardtii mutant, which is defective in the production of the PsaF subunit of PSI, provides an ideal platform for studying the processes involved in protecting PSI from excess light. This strain dies following the exposure to high light (HL) because of photo-oxidative damage. We used a second-site suppressor screen to identify genes involved in protecting PsaF-deficient PSI from excess light. In doing so, we demonstrated that the absence of the STT7 protein, which is required for LHCII phosphorylation and the process of state transitions suppresses the psaF HL-lethal phenotype. On the basis of chlorophyll fluorescence measurements, the psaF mutant has a more reduced plastoquinone pool at a given photosynthetic photon flux density than the wild-type cells. Under these conditions the process of state transitions will become active, resulting in the transfer of phosphorylated LHCII proteins to PSI, further increasing the excitation of PSI. However, in the psaF stt7 double mutant, the LHCII proteins will not be transferred to PSI, and thus the level of PSI excitation will remain lower. This study provides clear genetic evidence that the HL-lethal phenotype of the psaF mutant is because of PSI overexciation.