Fig. 3.

Photoregulation of carotenoid (Car) biosynthesis by blue (B), red (R), ultraviolet A (UV-A) and B (UV-B) light. Light-activated UV-B receptor (UVR8), cryptochromes (crys) and phytochromes (phys) inhibit COP1-based E3-ubiquitin-ligase and thus rescue HY5 transcription factor from proteolysis. Light-activated phys also inhibit PIF1 transcription factor. Phytoene synthase (PSY), the first and main rate-determining enzyme in the carotenoid biosynthesis pathway, is regulated by HY5 and PIF1 on the transcription level. Violaxanthin de-epoxidase (VDE) transcription is activated by HY5 as well. Low temperature increases HY5 binding with VDE and PSY promoters (Stanley and Yuan 2019). Light-dependent photosynthetic electron transport chain (ETC) decreases pH in lumen, increasing VDE activity. In addition, ETC differently changes the balance of reduced and oxidised plastoquinones (PQs): photosystem II (PSII) and plastidial NADH dehydrogenase (NDH) reduce PQ, and photosystem I (PSI) and plastidial terminal oxidase (PTOX) oxidise PQH₂. Desaturases (two desaturases, phytoene desaturase and ζ-carotene desaturase, catalyse four desaturations from phytoene to lycopene) use oxidised plastoquinone as an electron acceptor for the desaturation reactions (Ruiz-Sola and Rodríguez-Concepción 2012). Zeaxanthin (Zea) is a major Car for photodamage protection in the photosynthetic apparatus. Zea level depends both on the activity of β-carotene hydroxylase, which converts β-carotene to zeaxanthin in the common Car biosynthetic pathway, and on the activity of VDE, which converts violaxanthin back to zeaxanthin (Stanley and Yuan 2019). Light quality regulates the expression of both these enzymes, and light, via lumen acidification, activates VDE post-translationally. Gene names in italics and double lines — regulation at transcription level, regular — regulation at post-translation level — protein level and/or activity