Abstract
The photosystem II (PSII) activity of C3 plants is usually inhibited at noon associated with high light but can be repaired fast in the afternoon. However, the diurnal variation of photosystem I (PSI) activity is unknown. Although, cyclic electron flow (CEF) has been documented as an important mechanism for photosynthesis, the diurnal variation of CEF in sun leaves is little known. We determined the diurnal changes in PSI and PSII activities, light energy dissipation in PSII and the P700 redox state in two tropical tree species Erythrophleum guineense and Khaya ivorensis grown in an open field. The PSI activity (as indicated by the maximum quantity of photo-oxidizable P700) was maintained stable during the daytime. CEF was strongly activated under high light at noon, accompanying with high levels of non-photochemical quenching (NPQ) and PSI oxidation ratio. In the afternoon, CEF was maintained at a relatively high level under low light, which was accompanied with low levels of NPQ and P700 oxidation ratio. These results indicated that CEF was flexibly modulated during daytime under fluctuating light conditions. Under high light at noon, CEF-dependent generation of proton gradient across the thylakoid membranes (ΔpH) mainly contributed to photoprotection for PSI and PSII. By comparison, at low light in the afternoon, the CEF-dependent formation of ΔpH may be important for PSII repair via an additional ATP synthesis.
Highlights
Light is the driving force for photosynthesis
The fraction of overall P700 that cannot be oxidized in a given state [Y(NA)] was maintained at a low level of approximately 0.1 under high light in the two species (Figures 2E,F)
Three methods for the determination of cyclic electron flow (CEF) activity have been proposed and all depend on the exact determination of the P700 turnover rate (Miyake, 2010)
Summary
Excess light excitation could lead to photoinhibition (Powles, 1984; Barber and Andersson, 1992; Aro et al, 1993). High light stress usually causes selective photoinhibition of photosystem II (PSII; Barber and Andersson, 1992; Prasil et al, 1992; Asada, 1996, 1999). Photoinhibition of PSII occurs only when the rate of photodamage to PSII exceeds the rate of its repair (Aro et al, 1993; Murata et al, 2007; Takahashi and Murata, 2008; Takahashi et al, 2009). It has been indicated that the ROS accelerate PSII photoinhibition mainly through inhibition of the repair of photodamaged PSII (Nishiyama et al, 2001, 2004), some exceptions indicate that ROS cause direct photodamage
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