Jasmonate pathway regulates sphingolipid desaturation during cold stress.

In response to chilling, plants undergo a variety of metabolic changes, including structural modifications of sphingolipids, which have an important but poorly understood effect on cold tolerance. Here, we used biochemical, molecular, cell biological, and genetic approaches to investigate the mechanism of cold-induced sphingolipid regulation. Chilling stress affected sphingolipid metabolism in Arabidopsis thaliana, resulting in increased long-chain base (LCB) unsaturation by promoting the expression of the sphingoid LCB ∆8 desaturase gene SLD1. The sld1-1 mutant showed decreased Chl content, reduced plasma membrane fluidity, and growth inhibition under chilling stress. LCB ∆8 double-bond formation during cold stress was regulated by the jasmonate (JA) pathway, and the loss of the JA receptor CORONATINE INSENSITIVE1 (COI1) caused a decrease in LCB unsaturation. The JA pathway master transcription factor MYC2 directly targeted the SLD1 promoter to regulate its transcription. MYC2 also regulates the expression of C-REPEAT BINDING FACTORs (CBFs) and INDUCER OF CBF EXPRESSION1 (ICE1), which play pivotal roles in the cold stress response. Our results reveal the mechanism by which the JA pathway mediates sphingolipid metabolism during cold stress, providing insights into the underlying mechanism of lipid function in cold tolerance.