Abstract

Flesh lignification is a typical chilling injury (CI) symptom of loquat fruit during cold storage. Calcium chloride (CaCl 2 ) could enhance chilling tolerance in loquat fruit, but the molecular mechanism is still not illuminated. In this study, CaCl 2 treatment could decrease the activities and genes expression of peroxidase (POD) laccase (LAC), and inhibit the increase in firmness and lignin accumulation, thereby alleviating chilling-induced lignification in loquat fruit. Additionally, CaCl 2 enhanced the calmodulin (CaM) content, free Ca 2+ distribution, EjCaM7 , and CaM binding transcription activator 3 ( EjCAMTA3 ) expression in loquat fruit during cold storage, indicating Ca 2+ /CaM-CAMTA might be played a key role in response to cold stress. Moreover, the EjCAMTA3 and EjCaM7 proteins were identified and characterized from loquat fruit. EjCAMTA3 bound to the CG-box in EjPOD64 and EjLAC12-like promoters to repress their transcription. Further analysis revealed that EjCaM7 interacted with EjCAMTA3 in a Ca 2+ -dependent manner, and this interaction enhanced the EjCAMTA3-mediated transcriptional repression of EjPOD64 and EjLAC12-like genes. Taken together, these findings suggested that CaCl 2 treatment alleviates chilling-induced lignification in loquat fruit, which probably via the synergistic role of EjCaM7 and EjCAMTA3 in the modulation of EjPOD64 and EjLAC12-like genes expression, leading to the repression of lignin polymerization.