CaCl2 mitigates chilling injury in loquat fruit via the CAMTA5-mediated transcriptional repression of membrane lipid degradation genes.

ABSTRACT

Loquat fruit is vulnerable to chilling injury (CI) under long-term low temperature storage. The application of calciumchloride (CaCl2) can alleviate CI in loquat fruit, however, the molecular mechanisms remain unclear. In this study, the loquat fruit were immersed in 1 % CaCl2 solution for 10 min and then stored at 1 ± 1 ℃ for 35 d. The results showed that CaCl2 treatment suppressed the increases in internal browning index, electrolyte leakage, and malonaldehyde content in loquat fruit under chilling stress. The internal browning index in CaCl2-treated loquat fruit was 33.34 % lower than that in the control at the end of storage. Meanwhile, CaCl2 treatment delayed the phospholipids degradation, and retained high level of unsaturated/saturated fatty acid ratio, which was 15.21 % higher than that in the control fruit at the end of storage. The CaCl2 treatment also decreased the enzymatic activities and gene expressions of phospholipase D (PLD), phospholipase C (PLC), and lipoxygenase (LOX) in loquat fruit during cold storage. Moreover, a calmodulin-binding transcription activator (CAMTA) transcription factor (TF), EjCAMTA5, was cloned from loquat fruit. The EjCAMTA5 expression was up-regulated by cold stress and CaCl2 treatment. Further investigation revealed that EjCAMTA5 directly bound to the promoters of EjPLC6-like and EjLOX5 to repress their transcription. Taken together, these findings implied that CaCl2 application could activate the EjCAMTA5-mediated transcriptional repression of EjPLC6-like and EjLOX5 genes, which contributed to delaying the degradation of membrane lipid and maintaining the integrity of cell membrane, thereby inhibiting the occurrence of browning in loquat fruit under chilling stress.