ECAP is a key negative regulator mediating different pathways to modulate salt stress-induced anthocyanin biosynthesis in Arabidopsis.

Anthocyanins are a subgroup of plant flavonoids with antioxidant activities and are often induced by various biotic and abiotic stresses in plants, probably to efficiently scavenge free radicals and reactive oxygen species. However, the regulatory mechanisms of salt stress-induced anthocyanin biosynthesis remain unclear. Using molecular and genetic techniques we demonstrated key roles of ECAP in differential salt-responsive anthocyanin biosynthesis pathways in Arabidopsis thaliana. ECAP, JAZ6/8 and TPR2 are known to form a transcriptional repressor complex, and negatively regulate jasmonate (JA)-responsive anthocyanin accumulation. In this study, we demonstrated that under moderate salt stress, the accumulation of anthocyanins is partially dependent on JA signaling, which degrades JAZ proteins but not ECAP. More interestingly, we found that high salinity rather than moderate salinity induces the degradation of ECAP through the 26S proteasome pathway, and this process is independent of JA signaling. Further analysis revealed that ECAP interacts with MYB75 (a transcription factor activating anthocyanin biosynthetic genes) and represses its transcriptional activity in the absence of high salinity. Our results indicated that plants adopt different strategies for fine-tuning anthocyanin accumulation under different levels of salt stress, and further elucidated the complex regulation of anthocyanin biosynthesis during plant development and responses to environmental stresses.