1-methylcyclopropene treatment improves chilling tolerance by regulating IAA biosynthesis, auxin signaling transduction and cell wall degradation in peach fruit

Abstract

Chilling injury (CI) is a major issue in peach fruit during cold storage, which can be alleviated by 1-methylcyclopropene (1-MCP) treatment. Previous works have focused on ethylene regualtion. Recently, auxin signals were found to play vital roles in both 1-MCP-regulated fruit ripening and cold resistance. However, the information regarding the relationship between auxin metabolism and 1-MCP-induced cold tolerance was still limited, especially in cold-sensitive fruit. To investigate the underlying mechanisms, we performed transcriptome analysis and found that 1-MCP treatment significantly regulated several metabolic pathways, including auxin signaling, cell wall pectin degradation, and indole pyruvate metabolism. This regulation contribute to the development of cold resistance by maintaining cell wall structural integrity through delaying the increase of water-soluble pectin (WSP) and the decrease of CDTA-soluble pectin (CSP) and sodium carbonate-soluble pectin (NSP). Accordingly, 1-MCP treatment reduced the activities of polygalacturonase (PG), pectin methylesterase (PME) and pectin lyase (PEL), and down-regulated the expressions of PpPG1, PpPG2, PpPME1, PpPME2, PpPEL1 and PpPEL2. Moreover, the treatment decreased indole-3-acetic acid (IAA) biosynthesis via the indole pyruvate pathway, which led to the attenuation of the auxin signaling pathway through down-regulation of auxin response factors (PpARF1), auxin-responsive genes (PpAUX/IAA1, PpSAUR1 and PpGH3–1), and auxin receptor proteins (PpTIR1) expressions. Our results suggested 1-MCP treatment improved chilling tolerance by regulating IAA biosynthesis, auxin signaling transduction and cell wall degradation, and provided new insight into the mechanisms of 1-MCP-induced cold resistance in postharvest peach fruit.