Although light is essential for photosynthesis, when in excess, it may
damage the photosynthetic apparatus, leading to a phenomenon known as
photoinhibition. Photoinhibition was thought as a light-induced damage
to photosystem II; however, it is now clear that even photosystem I may
become very vulnerable to light. One main characteristic of light
induced damage to photosystem II (PSII) is the increased turnover of the
reaction center protein, D1: when rate of degradation exceeds the rate
of synthesis, loss of PSII activity is observed. With respect to
photosystem I (PSI), an excess of electrons, instead of an excess of
light, may be very dangerous. Plants possess a number of mechanisms able
to prevent, or limit, such damages by safe thermal dissipation of light
energy (non-photochemical quenching, NPQ), slowing-down of electron
transfer through the intersystem transport chain
(photosynthesis-control, PSC) in co-operation with the Proton Gradient
Regulation (PGR) proteins, PGR5 and PGRL1, collectively called as
short-term photoprotection mechanisms, and the redistribution of light
between photosystems, called state transitions (responsible of
fluorescence quenching at PSII, qT), is superimposed to these short term
photoprotective mechanisms. In this manuscript we have generated a
number of higher order mutants by crossing genotypes carrying defects in
each of the short-term photoprotection mechanisms, with the final aim
to obtain a direct comparison of their role and efficiency in
photoprotection. We found that mutants carrying a defect in the
ΔpH-dependent photosynthesis-control are characterized by
photoinhibition of both photosystems, irrespectively of whether
PSBS-dependent NPQ or state transitions defects were present or not in
the same individual, demonstrating the primary role of PSC in
photoprotection. Moreover, mutants with a limited capability to develop a
strong PSBS-dependent NPQ, were characterized by a high turnover of the
D1 protein and high values of Y(NO), which might reflect energy
quenching processes occurring within the PSII reaction center.