‘Whangkeumbae’ (Pyrus pyrifolia) is a variety of sand pear fruit well-known for its smooth surface and good taste. However, the fruit quality is adversely affected by postharvest ethylene production. Therefore, improving postharvest shelf life by regulating fruit senescence is critical to promoting the ‘Whangkeumbae’ fruit industry. Here, we investigated the effect of salicylic acid (SA) spray on fruit senescence in sand pears during room temperature shelf life. Exogenous SA reduced polyphenol oxidase (PPO) activity and malondialdehyde (MDA) content during room temperature shelf life. Additionally, SA effectively maintained the fruit skin coloration and increased the activity of antioxidant enzymes, such as superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX). SA treatment inhibited PpPPO1 expression and upregulated PpSOD1, PpAPX6, and PpGST2 expression. Furthermore, SA application downregulated the expression of PpACO2, PpEIN3a, PpNCED1, and PpAOC2, while upregulating PpNPR-1, PpTAR2, and PpCOMT1 during room temperature shelf life. SA treatment also influenced cell wall metabolism and modification genes by inhibiting PpPG1, PpPME2, and PpCEL3 and inducing PpPGIP1 expression. Additionally, SA treatment affected sugar and acid metabolism genes and increased the expression of PpSPS1, PpSUS1, PpSOT1, PpTMT4, PpSWEET15, and PpcyNAD-MDH, but suppressed the expression of PpcyNADP-ME. The Pearson correlation analysis indicated that PPO activity and MDA content were positively correlated with the expression of PpPPO1, PpACO2, PpEIN3a, PpNCED1, PpAOC2, PpPG1, PpPME2, PpCEL3, and PpcyNDA-MDH. Conversely, these factors were negatively associated with the activities of SOD, POD, CAT, and APX, as well as the expression levels of PpSOD1, PpPOD1, PpCAT1, PpAPX6, PpGST2, PpNPR-1, PpTAR2, PpCOMT1, PpPGIP1, PpSPS1, PpSUS1, PpSOT1, PpTMT4, PpSWEET15, and PpcyNAD-MDH. Our results reveal that exogenous SA could delay fruit senescence in sand pear fruit by regulating various biochemical and molecular mechanisms and can be used to effectively extend fruit shelf life during room temperature storage. However, further research is necessary to determine whether the fruits sprayed with SA are suitable for direct human consumption.

The Prunus mume species has undergone a long process of domestication and introduction in China, resulting in marked differences in freezing tolerance among populations across a latitudinal gradient of approximately 1,000 km. However, the introduction and domestication process is time-consuming, constraining the efficiency of species introduction. In this study, P. mume samples with the same genetic background spanning over 1,000 km from north to south were selected as experimental materials. The molecular mechanisms underlying cold-acclimation-mediated freeze tolerance in P. mume were investigated using multiomics high-throughput sequencing and molecular biology techniques. The cold-acclimated plant material exhibited enhanced freezing tolerance. Cold acclimation substantially enhanced transcriptional reprogramming under cold stress, accompanied by the remodeling of chromatin states in the promoter region. A variety of cis-regulatory elements were identified in the open chromatin regions of cold-acclimated plant materials, including G-box, ABRE, and other stress-responsive elements. The bZIP transcription factor PmGBF1, as a key regulatory node, directly regulates the expression of the cold shock protein gene PmCSL by binding to G-box elements to regulate freezing tolerance. This study reveals the molecular mechanism underlying cold acclimation mediated by the PmGBF1-PmCSL pathway in regulating P. mume freezing tolerance, providing an epigenetic theoretical basis and genetic resources for cold-acclimation breeding of freezing tolerance in woody plants.

Iron deficiency chlorosis severely limits the productivity of ‘Yali’ pears in alkaline soils. This study systematically investigated the physiological and molecular responses of ‘Yali’ pears to varying degrees of iron deficiency, focusing on the roles of PbFRO2 (Pyrus bretschneideri Ferric Reductase Oxidase 2), PbIRT1 (Pyrus bretschneideri Iron-Regulated Transporter 1), and PbCS2 (Pyrus bretschneideri Citrate Synthase 2) in iron uptake and homeostasis. Based on field observations, pear trees were categorized into normal, moderately chlorotic, and severely chlorotic groups. Results demonstrated that moderate iron deficiency upregulated PbFRO2 (2.86–7.09-fold), enhanced root ferric reductase (FCR) activity, and promoted Fe³⁺ reduction and Fe²⁺ transport. In contrast, severe deficiency suppressed the expression of these genes and reduced photosynthetic efficiency. Leaf citrate content significantly increased with chlorosis severity, while root citrate content exhibited seasonal fluctuations, peaking in July. Multivariate analyses (PCA and PLS-DA) revealed distinct physiological clustering: normal and moderately chlorotic groups overlapped, whereas the severely chlorotic group formed a separate cluster, reflecting a transition from compensatory activation to metabolic collapse. PbFRO2 emerged as a central regulator, driving root iron storage in spring and redistribution in summer. These findings elucidate a biphasic adaptation strategy, where moderate deficiency triggers gene-mediated iron mobilization, whereas severe stress disrupts homeostasis. This study provides critical insights into iron metabolism dynamics and proposes PbFRO2 as a molecular target for breeding iron-efficient pear cultivars.

Sand pear quality is limited by rapid postharvest senescence driven by ethylene. We identify two Ethylene Response Factors with opposing functions in this process. PpERF061 is induced by salicylic acid (SA) and repressed by the ethylene precursor ACC. Gain- and loss-of-function assays show that PpERF061 delays senescence by repressing ethylene biosynthesis and cell wall-modifying genes (PpACO3, PpPG1). PpERF061 also interacts with the NAC transcription factor PpNAC14, placing it within a broader regulatory module. In contrast, PpERF51B-L promotes senescence via two mechanisms: it forms a repressive complex with PpNAC14 to suppress PpERF061, and it engages ethylene signaling by interacting with PpEIN3a/b, with transcriptional activation by PpEIN3a. Notably, the SA receptor NPR1 attenuates PpERF51B-L’s pro-senescence activity through protein-protein interaction, revealing an SA-ethylene antagonism at the ERF node. These findings provide a mechanistic framework for manipulating hormonal crosstalk to extend shelf life and improve marketability in sand pear.