How UV-B-activated UVR8 triggers LOX1 to close stomata: Unveiling a mechanism of photoreceptor-regulated enzyme activity in the cytoplasm

UV-B radiation (280-315 nm), a high-energy component of sunlight, is partially absorbed by the ozone layer before reaching the Earth's surface.Its intensity at ground level varies significantly across different locations and times of day, influenced by latitude, altitude, and seasonal changes.Perceived by the photoreceptor UVR8, low-dose UV-B regulates multiple physiological processes in plants, including promoting photomorphogenesis, enhancing the accumulation of flavonoids and anthocyanins to alleviate oxidative damage, and modulating stomatal aperture (Podolec et al. 2021).Stomatal aperture is regulated by multiple environmental and internal factors, including light, humidity, CO concentration, and phytohormones such as abscisic acid (Lawson and Matthews, 2020).While studies have shown that low doses of UV-B promote stomatal closure, the underlying molecular mechanisms remain unclear.In new work, Yan Liu, Jue Wang, and collaborators (Liu et al. 2025) found that UV-B-activated UVR8 directly interacts with lipoxygenase LOX1, enhancing its non -heme iron-containing dioxygenase activity and leading to an increase in oxylipin derivatives that promote stomatal closure.This process functions upstream of stomatal closure mediated by salicylic acid (SA).The authors demonstrated that UV-B-induced stomatal closure in Arabidopsis (A. thaliana) primarily depends on UVR8 expression in the epidermis.Lipid profiling revealed significant UV-B-induced accumulation of the two most abundant polyunsaturated fatty acids linoleic acid and linolenic acid in a UVR8dependent manner.This process involves the plastid-localized phospholipase A1 enzymes PLIP1 and PLIP3.However, whether UV-B light regulates PLIP1 and PLIP3 protein levels or activities through UVR8 remained unclear.Although exogenous application of linoleic acid or -linolenic acid induces stomatal closure in the Col-0 accession, this effect was abolished in the uvr8-6 mutant, regardless of UV-B exposure.Further investigation revealed that 9-keto-10(E),12(Z),15(Z)-octadecatrienoic acid (9-KOTE), an oxidative metabolite