Abstract
Photoinhibition was defined originally as the decrease in photosynthetic activity that occurs upon excess illumination. The site of photoinhibition has generally been considered to be located in PSII. However, a novel type of photoinhibition has been characterized in chilling-sensitive plants, and subsequently also in chilling-tolerant plants. This photoinhibition occurs under relatively weak illumination at chilling temperatures and the main site of damage is in PSI. The photoinhibition of PSI involves the inactivation of the acceptor side (iron-sulfur centers) and the degradation of the psaA/B gene products, which are hetero-dimer subunits of the PSI reaction center complex. Chilling stress, the presence of oxygen and the reducing pressure from PSII are characteristic requirements for the photoinhibition of PSI in vivo. The inhibition seems to be induced by the reactive oxygen species produced under chilling conditions. Since electron transfer from PSII is essential for the photoinhibition of PSI, the photoinhibition of PSII under high light may protect PSI from photoinhibition. On the other hand, photoinhibition of PSI results in the reduction of electron carriers between PSI and PSII (i.e. high excitation pressure) leading the enhanced rate of PSII photoinhibition. Thus, photoinhibition of PSII and PSI must affect each other.
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