Postharvest losses of fruits and vegetables present a major challenge in developing countries due to limited infrastructure and widespread use of synthetic chemicals, leading to food waste, economic decline, and health hazards. Plant extracts rich in bioactive compounds such as phenolics, flavonoids, alkaloids, and essential oils have emerged as promising, eco-friendly options for preserving and improving the quality of horticultural crops after harvest. This overview consolidates current knowledge on the chemical diversity, functional applications, and cellular mechanisms of plant extracts in preventing spoilage, slowing ripening, and maintaining the nutritional and sensory qualities of fruits and vegetables. Comparative analyses in selected developing nations highlight the seriousness of postharvest losses and the necessity for environmentally sustainable solutions. The review examines recent advancements, practical applications, and challenges like performance inconsistency, standardization, and scalability related to the use of botanical extracts. Future outlooks focus on integrating plant extracts with emerging technologies and ensuring these solutions reach smallholder farmers. Overall, plant extracts offer a sustainable route to environmentally friendly and safer postharvest management, which can bolster food security and foster responsible agriculture in the developing world. To unlock their full potential, further research should aim to develop standardized extraction techniques, optimize formulations, and enhance policy and technological support for large-scale implementation in developing countries.
Citrus yellow vein clearing virus (CYVCV) is the causative agent of the yellow vein clearing disease (YVCD), a worldwide and highly destructive disease in lemon (Citrus lemon) and sour orange trees (C. aurantium). The typical symptoms of vein clearing are believed to be associated with CYVCV infection in citrus, so virus-specific diagnostic systems are currently used to confirm infection. In the present study, virome analysis based on high-throughput sequencing (HTS) on a lemon plant showing YVCD revealed mixed infection of CYVCV, iris domestica betaflexyviridae 1 (IDBV), and hop stunt viroid (HSVd). This multiple infection was confirmed in other two lemon plants with similar symptoms using virus/viroid specific primers. This is the first report of IDBV in lemon. Through molecular characterization and the reconstruction of phylogenetic relationships, a possible origin of the viruses/viroid identified in lemon has been hypothesized. Such mixed infections raise new questions about their role in the expression of YVCD symptoms observed on lemon.
Prion diseases are fatal and contagious brain disorders caused by a pathogenic prion protein (PrPSc) derived from the benign prion protein (PrPC). To date, there are no therapeutic substances to completely block prion diseases. Thus, the development of a therapeutic substance is necessary, and the identification of a novel biomarker of prion disease is the first essential step to develop new drugs. In the present study, we carried out a metagenomic analysis to identify microbiome biomarkers for prion disease using next-generation sequencing and bioinformatics tools in intraperitoneally prion-infected mice. In addition, we evaluated the protective effects of epigallocatechin-3-gallate (EGCG), a potent microbiome changer, in prion-infected mice by western blotting and survival analysis. We found a total of 14 differentially abundant taxa between prion-infected and control mice. In addition, we found that prion diseases caused altered microbiome networks and upregulation of DNA repair-related pathways. Furthermore, we observed the protective effect of the microbiome changer EGCG against prion disease in prion-infected mice. Given previous reports of microbiome alterations in prion diseases, we further validated these associations and demonstrated the protective effects of a microbiome-modulating compound.
Cannabinoid content can vary several-fold across Cannabis sativa L. cultivars that carry functional, closely related CBDA synthase (CBDAS) and THCA synthase (THCAS) alleles, a difference that coding-sequence variation among functional alleles does not fully explain. Structural and copy-number variation at the synthase loci, the functional or pseudogenised state of synthase alleles, and linkage at the B locus account for much of the qualitative drug-versus-hemp chemotype; however, these genetic factors do not fully explain the quantitative, several-fold variation in cannabinoid content among cultivars that carry functional, near-identical synthase alleles. Three independent lines of evidence now indicate that chromatin-level regulation contributes to this variation. H3K4me3 and H3K56ac co-occupy the promoters and gene bodies of THCAS, CBDAS, OLS, and OAC exclusively in glandular trichome tissue while H3K27me3 marks the identical loci in vegetative tissues, indicating that a Polycomb-to-Trithorax chromatin switch is associated with trichome-specific cannabinoid gene expression, potentially independently of transcription factor availability. Progressive DNA hypomethylation accumulates during micropropagation in a cultivar-specific manner, with promoter-region differentially methylated positions reaching up to 22% by twenty subcultures, identifying DNA methylation maintenance as a candidate determinant of epigenetic stability in clonally propagated material, although the functional consequences for cannabinoid pathway gene expression and yield remain to be quantitatively established. In Cannabis indica cell suspension cultures, UV irradiation increases genome-wide DNA methylation (detected by MSAP, which does not resolve locus-specific changes) and elevates CBDAS transcript levels approximately 4-fold relative to non-irradiated controls. This coupling of an environmentally triggered methylation change to cannabinoid pathway gene expression in the Cannabis genus is suggestive, but the genome-wide MSAP signal and the use of C. indica cell cultures mean the locus-specific methylation change at the CBDAS promoter remains to be demonstrated. These findings identify specific, experimentally documented chromatin states as candidate targets for dCas9-effector intervention, including the H3K27me3 repressive state at cannabinoid loci that could be addressed by dCas9-KDM6A and the propagation-induced CG hypomethylation that could be addressed by dCas9-DNMT3A; these editing strategies remain hypotheses that have not yet been tested in Cannabis. We synthesize functional evidence from Catharanthus roseus, Papaver somniferum, and Artemisia annua demonstrating that equivalent chromatin switches control secondary metabolite yield in medicinal plants, evaluate which dCas9-effector architectures are most appropriate for each Cannabis chromatin target, and identify the critical mechanistic gaps that must be closed before epigenome editing can be rationally deployed for cannabinoid yield enhancement in Cannabis.
