Abstract
To understand whether arginine catabolism might be involved in hot air (HA)-induced chilling tolerance mechanism in tomato fruit, we investigated the effect of HA treatment on endogenous arginine catabolism in relation to chilling injury. Tomato fruit were harvested at mature green stage and treated with HA at 38°C for 12 h and then stored at 2°C for 21 days. The effects of HA treatment on fruit chilling injury and gene expression levels or enzyme activity, and metabolites related to arginine catabolism were evaluated. HA treatment reduced the chilling injury symptoms of tomato fruit and enhanced the accumulation of endogenous polyamines, especially putrescine and proline. This accumulation is associated with the increased transcript levels of genes encoding arginase (LeARG1 and LeARG2), arginine decarboxylase (LeADC), ornithine decarboxylase (LeODC) and ornithine aminotransferase (LeOAT) at most sampling times. However, HA treatment had little effect on nitric oxide synthase activity and nitric oxide concentration. These results revealed that the reduction in chilling injury by HA treatment may be due to the accumulation of putrescine and proline induced primarily by activating the catabolism of endogenous arginine.
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