β-cyclocitral upregulates salicylic acid signalling to enhance excess light acclimation in Arabidopsis.

β-cyclocitral (β-CC), a volatile oxidized derivative of β-carotene, can upregulate the expression of defence genes to enhance excess light (EL) acclimation. However, the signalling cascades underlying this process remain unclear. In this study, salicylic acid (SA) is involved in alleviating damage to promote β-CC-enhanced EL acclimation. In early stages of EL illumination, β-CC pretreatment induced SA accumulation and impeded reactive oxygen species (ROS) production in the chloroplast. A comparative analysis of two SA synthesis pathways in Arabidopsis revealed that SA concentration mainly increased via the isochorismate synthase 1 (ICS1)-mediated isochorismate pathway, which depended on essential regulative function of enhanced disease susceptibility 1 (EDS1). Further results showed that, in the process of β-CC-enhanced EL acclimation, nuclear localization of nonexpressor of pathogenesis-related genes 1 (NPR1) was regulated by SA accumulation and NPR1 induced subsequent transcriptional reprogramming of gluthathione-S-transferase 5 (GST5) and GST13 implicated in detoxification. In summary, β-CC-induced SA synthesis contributes to EL acclimation response by decreasing ROS production in the chloroplast, promoting nuclear localization of NPR1, and upregulating GST transcriptional expression. This process is a possible molecular regulative mechanism of β-CC-enhanced EL acclimation.