Eggplant is a vegetable crop with high economic value that is cultivated worldwide. The dwarf mutant is an important germplasm material that has been extensively used in crop breeding. However, no eggplant dwarf mutants have been reported, and little is known regarding the genes responsible for dwarfism in eggplant. In this study, we isolated an eggplant dwarf mutant (dwf) from an ethyl methyl sulfonate (EMS)-induced mutant library. Genetic analysis revealed that dwf was caused by a single recessive gene. A candidate gene SmCPR1, encoding cytochrome P450 reductases (CPR1), was identified by bulked segregant analysis (BSA). Mutation from G to A at 8216 bp of SmCPR1 resulted in mutation of the amino acid from valine to isoleucine. The results of KASP and Sanger sequencing further support the conclusion that SmCPR1 is a candidate gene responsible for the dwarfism of dwf. Moreover, the activity of SmCPR1 was significantly increased in dwf, which might be a response to dwarfism in dwf.

Dwarfism is a desirable trait in eggplant breeding, as it confers higher lodging resistance and allows simplified management and harvest. However, a few dwarf mutants have been reported, and the molecular mechanism underlying dwarfism in eggplant is completely unknown. Here, we report a dwarf mutant (dwf) isolated from an ethyl methyl sulfonate (EMS)-induced mutant library. The hypocotyl length, plant height, and length of internode cells of dwf were significantly decreased compared to those of the wild-type parent ‘14-345’ (WT). Differential gene expression analysis revealed that GA-related genes, including GA2ox and DELLA, were up-regulated whereas the gibberellin (GA₃) content decreased in dwf. Moreover, exogenous GA₃ treatment significantly increased the relative growth rate of dwf compared to WT, further indicating the important roles of GA in regulating the dwarf phenotype of dwf. Collectively, our findings shed light on GA-mediated dwarfism in dwf plants and offer a good germplasm that could be used for eggplant dwarfism breeding in the future.

Leaf size is a crucial trait in eggplant breeding, as it influences photosynthesis, plant biomass and management. However, little is known about the molecular mechanism regulating leaf size in eggplant. This study reports a small leaf mutant (slf) generated with the mutagen ethyl methane sulfonate (EMS). The slf mutant showed restricted cell proliferation and an increased content of auxin. Transcriptome analysis revealed that several genes involved in auxin signaling are upregulated in slf. Exogenous application of auxinole, an auxin antagonist of TIR1/AFB receptors, repressed the expression of these genes and restored leaf growth of slf, suggesting that the small leaf size of slf is likely associated with auxin signaling. This study provides essential clues to unveil the molecular mechanism of leaf size regulation in eggplant.

Ganoderma lucidum spores are widely consumed natural functional materials; however, the influence of sporoderm disruption on the physicochemical characteristics and biological performance of spore polysaccharides remains insufficiently understood. In this study, polysaccharides extracted from intact spores (GLSP-I) and sporoderm-broken spores (GLSP-SB) were systematically compared to clarify how industrial processing affects their physicochemical properties and cytoprotective activity. Chemical characterization demonstrated that sporoderm disruption increased extraction yield and modified molecular weight distribution, monosaccharide composition, and spectroscopic features without fundamentally altering the polysaccharide backbone. Both polysaccharide fractions alleviated TBHP-induced oxidative injury, whereas GLSP-SB exhibited enhanced cytoprotective efficacy. Quantitative proteomic analysis revealed that GLSP-SB regulated a broader set of proteins associated with mitochondrial organization, oxidative stress response, autophagy, and cellular energy metabolism. Functional assays further showed that GLSP-SB promoted mitochondrial biogenesis, restored ATP production, and maintained mitochondrial morphology under oxidative stress conditions. Mechanistic validation demonstrated activation of the SIRT1/AMPK signaling pathway, indicating that modulation of this pathway contributes to mitochondrial adaptive responses. These findings suggest that sporoderm disruption reshapes polysaccharide characteristics and is associated with enhanced mitochondrial protective activity, providing mechanistic insight into the rational processing and functional utilization of G. lucidum spore products.

Research on high-quality Atractylodes chinensis (DC.) Koidz. germplasm is pivotal for its standardized cultivation, but the multi-omics mechanisms governing its plant architecture remain unclear. In this study, we integrated morphological quantification, RNA sequencing (RNA-seq), and liquid chromatography-tandem mass spectrometry (LC-MS/MS) to explore the molecular basis of architectural differences between a naturally compact line (JC) and the wild-type (WT). Morphological analysis confirmed that the JC line is characterized by significantly shorter internodes and increased branching compared to the WT. Transcriptomic analysis identified 7,271 differentially expressed genes (DEGs), specifically the downregulation of the gibberellin (GA) biosynthetic gene ent-kaurenoic acid oxidase ( KAO ) and the upregulation of the GA catabolic gene GA 2-oxidase ( GA2ox ) in the JC line. Parallel metabolomic profiling identified an accumulation of GA metabolic precursors (GA ₉ , GA ₁₉ , and GA ₄₄ ) and significantly higher cytokinin (CTK) content in JC relative to WT. These results suggest a GA-centric regulatory network where disrupted GA metabolism and enhanced CTK accumulation synergistically drive the compact architectural phenotype. This study elucidates the GA–CTK regulatory module as a core mechanism modulating internode elongation and branching, providing key candidate genes and foundational insights for the molecular breeding of elite A. chinensis germplasm.