Abstract

During outdoor mass cultivation, Haematococcus pluvialis cells, especially at the green motile stage, are frequently exposed to high light. However, the photoprotective mechanisms in H. pluvialis have not been well characterized. This study aimed to confirm the photoprotection of chlororespiration in H. pluvialis at the green motile stage. Under high light, inhibition of plastid terminal oxidase (PTOX), a key enzyme of chlororespiration, increased the relative variable fluorescence at the I-step (VI), causing a decrease in the plastoquinone (PQ) pool, which further led to photosystem II (PSII) acceptor side over-reduction. This condition disturbed the balance between light absorption and energy utilization, causing the over-excitation of PSII reaction centers, which was indicated by the fact that the inhibition of PTOX increased the relative variable fluorescence at the J-step (VJ) and the light absorption flux per active reaction center (ABS/RC), but decreased the electron transport flux per active reaction center (ETo/RC) in H. pluvialis. The over-reduction of the PSII acceptor side and the over-excitation of PSII reaction centers inevitably caused more severe photoinhibition as shown by a decrease in Fv/Fm (maximal photochemical efficiency of PSII). Furthermore, the level of photoinhibition was not changed when the PTOX was inhibited in the presence of the photodamaged-PSII repair inhibitor chloramphenicol, indicating that the inhibition of PTOX did not accelerate the photodamage to PSII directly. The above results suggest that the chlororespiration pathway protects H. pluvialis at the green motile stage against photoinhibition by decreasing the inhibition of the photodamaged-PSII repair mechanism.

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