Sugar level is an important determinant of fruit taste and consumer preferences. However, upstream regulators that control sugar accumulation during fruit maturation are poorly understood. In the present work, we found that glucose is the main sugar in mature pitaya (Hylocereus) fruit, followed by fructose and sucrose. Expression levels of two sucrose-hydrolyzing enzyme genes HpINV2 and HpSuSy1 obviously increased during fruit maturation, which were correlated well with the elevated accumulation of glucose and fructose. A WRKY transcription factor HpWRKY3 was further identified as the putative binding protein of the HpINV2 and HpSuSy1 promoters by yeast one-hybrid and gel mobility shift assays. HpWRKY3 was localized exclusively in the nucleus and possessed trans-activation ability. HpWRKY3 exhibited the similar expression pattern with HpINV2 and HpSuSy1. Finally, transient expression assays in tobacco leaves showed that HpWRKY3 activated the expressions of HpINV2 and HpSuSy1. Taken together, we propose that HpWRKY3 is associated with pitaya fruit sugar accumulation by activating the transcriptions of sucrose metabolic genes. Our findings thus shed light on the transcriptional mechanism that regulates the sugar accumulation during pitaya fruit quality formation.

The performance of p-Anisaldehyde (PAA) for preserving pitaya fruit quality and the underpinning regulatory mechanism were investigated in this study. Results showed that PAA treatment significantly reduced fruit decay, weight loss and loss of firmness, and maintained higher content of total soluble solids, betacyanins, betaxanthins, total phenolics and flavonoids in postharvest pitaya fruits. Compared with control, the increase in hydrogen peroxide (H₂O₂) content and superoxide anion (O₂^•−) production was inhibited in fruit treated with PAA. Meanwhile, PAA significantly improved the activity of antioxidant enzymes superoxide dismutase (SOD), peroxidase (POD) and catalase (CAT). Moreover, PAA-treated pitaya fruit maintained higher ascorbic acid (AsA) and reduced-glutathione (GSH) content but lower dehydroascorbate (DHA) and oxidized glutathione (GSSG) content, thus sustaining higher ratio of AsA/DHA and GSH/GSSG. In addition, activities of ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR) and dehydrogenation ascorbic acid reductase (DHAR), as well as the expression of HpSOD, HpPOD, HpCAT, HpAPX, HpGR, HpDHAR and HpMDHAR, were enhanced after PAA treatment. The findings suggest that postharvest application of PAA may be a reliable method to control postharvest decay and preserve quality of harvested pitaya fruit by enhancing the antioxidant potential of the AsA-GSH cycle and activating an antioxidant defense system to alleviate reactive oxygen species (ROS) accumulation.

Highly prized for its unique taste and appearance, pitaya is a tasty, low-calorie fruit. It has a high-water content, a high metabolism, and a high susceptibility to pathogens, resulting in an irreversible process of tissue degeneration or quality degradation and eventual loss of commercial value, leading to economic loss. High quality fruits are a key guarantee for the healthy development of economic advantages. However, the understanding of postharvest conservation technology and the regulation of maturation, and senescence of pitaya are lacking. To better understand the means of postharvest storage of pitaya, extend the shelf life of pitaya fruit and prospect the postharvest storage technology, this paper analyzes and compares the postharvest quality changes of pitaya fruit, preservation technology, and senescence regulation mechanisms. This study provides research directions for the development of postharvest storage and preservation technology.

Decay caused by Neopestalotiopsis clavispora is an important postharvest disease of blueberries that seriously affects the commercial value of blueberry fruit. In this paper, we studied the inhibitory activity and mode of action of thymol against the pathogenic fungus of blueberries caused by Neopestalotiopsis clavispora. The results demonstrated that thymol administration could limit mycelial growth in vitro; the inhibitory effect was positively connected with thymol mass concentrations, and the minimal inhibitory concentration (MIC) was 100 mg/L. Further investigations revealed that MIC thymol treatment dramatically reduced the germination of pathogenic spores and led to an increase in the conductivity of the pathogen, leakage of contents, and a decrease in pH. Propidium iodide (PI) staining experiments demonstrated that MIC thymol caused damage to mycelial cell membranes. Additionally, MIC thymol treatment promoted mycelium malondialdehyde content accumulation, inhibited superoxide dismutase (SOD) and catalase (CAT) enzyme activities, decreased adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) content and energy charge levels, and the fluorescence intensity of mycelium caused by MIC thymol treatment was significantly increased by the 2,7-Dichlorodi-hydrofluorescein diacetate (DCFH-DA) assay. The results of this study indicate that thymol suppresses the proliferation of Neopestalotiopsis clavispora by compromising the integrity of their cell membranes, promoting the accumulation of cellular reactive oxygen species (ROS), and interfering with energy metabolism.