The mechanism of photosystem‐ II inactivation during sulphur deprivation‐induced H 2 production in Chlamydomonas reinhardtii
Autor: | Szilvia Z. Tóth, Anna Podmaniczki, Valéria Nagy, Gábor Rákhely, Laura Zsigmond, Klára Szentmihályi, László Kovács, André Vidal-Meireles |
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Rok vydání: | 2018 |
Předmět: |
inorganic chemicals
0106 biological sciences 0301 basic medicine Photosynthetic reaction centre Hydrogenase Photosystem II Singlet oxygen digestive oral and skin physiology Chlamydomonas Chlamydomonas reinhardtii macromolecular substances Cell Biology Plant Science Biology Photosynthesis biology.organism_classification 01 natural sciences Electron transport chain 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology chemistry Genetics Biophysics 010606 plant biology & botany |
Zdroj: | The Plant Journal. 94:548-561 |
ISSN: | 1365-313X 0960-7412 |
DOI: | 10.1111/tpj.13878 |
Popis: | Sulphur limitation may restrain cell growth and viability. In the green alga, Chlamydomonas reinhardtii, sulphur limitation may induce H2 production lasting for several days, to be exploited as a renewable energy source. Sulphur limitation causes a large number of physiological changes, including the inactivation of photosystem II (PSII), leading to the establishment of hypoxia, essential for the increase in hydrogenase expression and activity. The inactivation of PSII has been long assumed to be caused by the sulphur-limited turnover of its reaction center protein, PsbA. Here we reinvestigated this issue in detail and show that i) upon transferring Chlamydomonas cells to sulphur-free media, the amount of cellular sulphur content decreases only by about 25%, ii) as demonstrated by lincomycin treatments, PsbA has a significant turnover and other photosynthetic subunits, namely RbcL and CP43, are degraded more rapidly than PsbA. On the other hand, sulphur limitation imposes oxidative stress early on, most probably involving the formation of singlet oxygen in PSII, which leads to an increase in the expression of GDP-L-galactose phosphorylase, playing an essential role in ascorbate biosynthesis. When accumulated to the millimolar concentration range, ascorbate may inactivate the oxygen-evolving complex and provide electrons to PSII albeit at a low rate. In the absence of a functional donor side and sufficient electron transport, PSII reaction centers get inactivated and degraded. We therefore demonstrate that the inactivation of PSII is a complex and multistep process, which may serve to mitigate the damaging effects of sulphur limitation. This article is protected by copyright. All rights reserved. |
Databáze: | OpenAIRE |
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