Programmed Cell Death as a Response to High Light, UV and Drought Stress in Plants - Abiotic Stress: Plant Responses and Applications in Agriculture - page 223

of chloroplasts. PSII is enriched in chlorophyll b molecules which results in a maximum ab‐
sorption at the orange/red light spectrum (650-680 nm), whereas, PSI is enriched in chloro‐
phyll a molecules and absorbs in the far red (700nm). The reaction centers of PSII and PSI
are coupled by a chain of electron carriers. A spectral imbalance of light may result in an
unequal excitation of two photosystems, leading to increased or decreased ROS production
[130]. Therefore, the distribution of light-absorbing antenna complexes between PSII and PSI
is under control and can be regulated through a short-term adaptation (e.g. state transition)
or long-term acclimation processes. State transition is a reversible phosphorylation of the
main LHCII protein and its migration between PSII and PSI [135,136]. Thylakoid-associated
kinase 1 (TAK1) is essential for this process since it is responsible for the phosphorylation of
thylakoid proteins [137]. In contrast, long-term responses employ modifications of the pho‐
tosynthetic complexes structure through the adjustment of LHCII and PSII size or PSI/PSII
ratio [138,139]. Both short-and long-term processes are triggered by the perception of imbal‐
anced photosystem excitation via redox signals that come from the photosynthetic electron
transport (PET) chain, especially from one of electron carriers - plastoquinone (PQ)
[130,140].
In natural environment, plants are often exposed to high light (HL) intensities that lead to
the absorption of more light energy than can be used for carbon dioxide fi xation [77]. The
amount of absorbed light energy that is excessive and cannot be used for photosynthetic me‐
tabolism is termed excess excitation energy (EEE) [77,130]. In response to EEE, there is an
immediate increase in the electron transport rate and in consequence redox changes of PET
components. Alterations in the redox status of PET, especially the reduction of PQ pool
leads to the expression deregulation of nuclear and chloroplastic genes that encode photo‐
synthesis components such as LHC proteins [141-143] and antioxidants like APX [144,145].
The response to EEE involves not only the alteration in photosynthetic fl ux but it is also ac‐
companied by changes in the water status and temperature of the leaf, and in consequence it
is associated with elevated ABA levels, changes in the redox state of glutathione pool and
increased activity of heat shock transcription factors [146,147]. If the accumulation of ROS
exceeds the ability of removing them by antioxidant systems, it may cause a photooxidative
damage of the photosynthetic apparatus which may lead to cell death, manifested by
bleaching, chlorosis or bronzing of leaves [148]. Therefore, the avoidance of EEE, its dissipa‐
tion and HL tolerance are fundamental for the plant survival. EEE-mediated PCD can be
considered as a beneficial process, as it triggers signal transduction to systemic cells and
their acclimation to high light [130,131].
Avoidance strategies include such processes as: movements of chloroplasts, decrease in the
number of photosynthetic reaction centers, curling of leaves and increase in the thickness of
cuticular wax [149]. During HL treatment, chloroplasts have been demonstrated to move to
the anticlinal wall (Figure 5) and this response has been proven to be mediated by blue/UVA
receptors [150].