Fig. 4.
Light-dependent components of non-photochemical quenching (NPQ) of chlorophyll a fluorescence. Photoregulation of NPQ by blue (B), red (R), green (G) and white (W) light. Photosynthetic electron transport chain (ETC) affects NPQ via lumen acidification (↓pHlumen) and via change of plastoquinone redox state (↑PQH2/PQ). Lumen acidification promotes PsbS protein protonation following disconnection of LHCII trimers from PSII and energy dissipation — this is the qE component of NPQ. Lumen acidification also promotes protonation and activation of the violaxanthin de-epoxidase (VDE) following violaxanthin (Viol) to zeaxanthin (Zea) conversion and energy dissipation by Zea — this is the qZ component of NPQ. Reduced plastoquinones via cytochrome b6f complex activate the serine/threonine kinase STN7, which phosphorylates the mobile antenna LHCII and thus induces its dissociation from PSII and relocation from granal to stromal thylakoids, reducing energy transfer to PSII — this is the qT component of NPQ. Light-induced destruction of PSII (primarily D1 protein) is responsible for the photoinhibition component qI. The qH component of NPQ is connected with the PSII antenna, and its mechanism is yet to be elucidated (dashed arrow). High-intensity (↑I) blue light induces chloroplast avoidance response, decreasing light absorption by Chls. However, the contribution of this process to NPQ and the existence of qM component are questionable (dashed arrow). Several protein effectors of NPQ (PSBS, VDE and PETA for cytf subunit of cytochrome b6f complex) are regulated by light at the transcriptional level, and the light of different quality induces these genes differently (shown based on data from Trojak and Skowron 2021). The mechanism of light regulation of VDE expression is shown in Fig. 3. Gene names in italics and double lines — regulation at transcription level, regular — regulation at post-translation level — protein level and/or activity