C-terminally encoded peptides (CEPs), a class of post-translationally modified peptides, have been discovered to be potential mediators of abiotic stress responses in several plants. In this study, to explore the possible roles of CEPs in blueberry salt and osmotic stress responses, a genome-wide identification of CEP genes was first conducted. In total, we identified 12 VcCEPs that can be further categorized into three subfamilies in blueberry. Collinearity analysis identified 14 segmental duplicated gene pairs involving four Subfamily I members and five Subfamily III members among VcCEPs, indicating that the expansion of the blueberry CEP gene family was promoted by the segmental duplication events of Subfamily I and Subfamily III members. Promoter analysis revealed that all the VcCEPs’ promoters contain drought-inducible and defence and stress-related elements, suggesting that they might contribute to the stress responses of blueberry. Gene expression analysis showed that, of the 12 VcCEPs, VcCEP1, VcCEP4, VcCEP5 and VcCEP6 expressed in blueberry root and/or leaf, with varied expression levels under salt and drought treatments, while others showed no expression or very low expression. We further identified CEP mature peptide (CEPm) sequences in VcCEPs, and found that nine VcCEPs contain one mature peptide, while VcCEP7, VcCEP2 and VcCEP10 contain 3, 2, and 2 mature peptide sequences, respectively. The CEPms of Subfamily III members (VcCEP7~11) share more than 60% similarity with reported stress-related CEP mature peptides from other plant species, indicating that they might function in blueberry stress responses. Additionally, exogenous application of different synthesized CEP mature peptides alleviated blueberry leaf yellowing/browning under 150 mM NaCl/500 mM mannitol treatments, with CEP7a*2 and CEP7a*2 + 7c showing the best effects. These findings indicate that their functions are concentration-dependent to some extent. Collectively, our study characterized the CEP genes in blueberry and can provide a basis for the future applications of CEPs in enhancing blueberry stress tolerance.

Fruit rot caused by Fusarium species represents a significant threat to watermelon (Citrullus lanatus (Thunb.) Matsum. et Nakai) quality and economic value. In this study, a fungal pathogen designated strain X2 was isolated from rotten watermelon fruit and identified as Fusarium proliferatum (Matsush.) Nirenberg ex Gerlach & Nir through integrated morphological, microscopic, and multi-locus molecular phylogenetic analyses. Koch’s postulates were fully satisfied, confirming that F. proliferatum strain X2 induces water-soaking and softening symptoms on watermelon fruit at relatively high temperatures. However, low-temperature storage at 4 °C strongly suppressed fungal growth and symptom development. Strain X2 produced fumonisins (FB1, FB2, and FB3) in vitro, but all of these mycotoxins were below the limit of detection in infected fruit tissues. Dual-culture assay revealed that three antagonistic Bacillus strains (G3-2, KP3P9 and K13C) can significantly inhibit the growth of F. proliferatum strain X2. Consistently, fruit co-inoculation assays verified that these strains differentially alleviated external and internal rot symptoms caused by the fungus. Biochemically, F. proliferatum strain X2 infection markedly increased cell wall-degrading enzyme (CWDE) activities, whereas co-inoculation with biocontrol Bacillus bacteria suppressed the activities of polygalacturonase (PG), pectin lyase (PL) and cellulase (CL) in a strain-specific manner. This study identified F. proliferatum strain X2 as a causal agent of watermelon fruit rot and highlights the roles of low-temperature storage and Bacillus-mediated biocontrol in disease suppression.