Apple EBF1 / CML15 – VQ8 module bridges ethylene and calcium signaling to modulate salt‐induced anthocyanin accumulation

Summary Although previous studies have shown that plants enhance salt tolerance by accumulating anthocyanins, the molecular mechanisms regulating salt stress‐induced anthocyanin biosynthesis remain unclear. This study establishes a regulatory network for salt‐induced anthocyanin accumulation in apple ( Malus × domestica ), centered on the VALINE–GLUTAMINE (VQ) protein MdVQ8. MdVQ8 promotes anthocyanin biosynthesis via a dual‐safeguard pathway: enhancing MdWRKY75‐mediated transcriptional activation of the key regulator MYELOBLASTOSIS 1 ( MdMYB1 ), and facilitating the TEOSINTE BRANCHED1/CYCLOIDEA/PCF 46 (MdTCP46)–MdMYB1 interaction. The calcium (Ca 2+ ) signaling regulator CALMODULIN‐LIKE PROTEIN 15 (MdCML15) maintains the MdVQ8–MdWRKY75 and MdVQ8–MdTCP46 complexes, thereby amplifying MdVQ8‐induced anthocyanin biosynthesis under salt stress. Additionally, the ethylene signaling repressor ETHYLENE INSENSITIVE3‐BINDING F‐BOX PROTEIN 1 (MdEBF1) counteracts MdVQ8 function by promoting its ubiquitination and degradation. Our findings reveal that the MdEBF1/MdCML15–MdVQ8 module coordinates the MdWRKY75– MdMYB1 and MdTCP46–MdMYB1 pathways to regulate salt‐induced anthocyanin accumulation. Therefore, these results offer new insights into the coordinated regulation of salt stress responses and anthocyanin biosynthesis by Ca 2+ and ethylene signaling.