Inactivation of the STT7 gene protects PsaF-deficient Chlamydomonas reinhardtii cells from oxidative stress under high light

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...

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Bibliographic Details
Published in:	Physiologia plantarum Vol. 141; no. 2; pp. 188 - 196
Main Authors:	Berry, Lindsay L, Brzezowski, Pawel, Wilson, Kenneth E
Format:	Journal Article
Language:	English
Published:	Oxford, UK Blackwell Publishing Ltd 01-02-2011 Blackwell
Subjects:	Biological and medical sciences Chlamydomonas reinhardtii Chlamydomonas reinhardtii - genetics Chlamydomonas reinhardtii - metabolism Chlamydomonas reinhardtii - radiation effects Chlorophyll Electron transport chain Energy Fluorescence Fundamental and applied biological sciences. Psychology LHCII protein Light Light effects Oxidation-Reduction - radiation effects Oxidative stress Oxidative Stress - radiation effects Phosphorylation Photons Photosystem I Photosystem II Plant physiology and development Plant Proteins - genetics plastoquinones Oxidative stress Chlorophyta Gene Plant physiology Algae Chlamydomonas reinhardtii Deficiency Light Chlorophyceae Inactivation Cell
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Summary:	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.
Bibliography:	http://dx.doi.org/10.1111/j.1399-3054.2010.01421.x ArticleID:PPL1421 ark:/67375/WNG-T8SFQX7S-L istex:F2D75DA3F7368ECEFE441BDA1F3DBDB9D977653D ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1
ISSN:	0031-9317 1399-3054
DOI:	10.1111/j.1399-3054.2010.01421.x