Integrated physiological, multi-omics analyses reveal key factors underlying seed abortion in Dimocarpus longan

Embryo abortion severely limits fruit set and yield stability in longan (<i>Dimocarpus longan</i>), yet the upstream physiological triggers and coordinated molecular program remain incompletely defined. Here, we characterized normal seed-forming (NF) and aborted seed-forming (AF) fruits at the critical abortion window by integrating phenotyping, mineral nutrient profiling, embryo-targeted RNA sequencing, and quantitative proteomics, followed by cross-omics association analyses. Orchards with high abortion incidence exhibited markedly low available boron, and aborted embryos displayed a distinctive nutrient-partitioning pattern characterized by severe embryonic boron depletion despite broad changes in other elements. Transcriptome analysis identified 3,865 differentially expressed genes (1,993 upregulated and 1,872 downregulated in AF), with enrichment in pathways related to phenylpropanoid biosynthesis, starch and sucrose metabolism, amino sugar and nucleotide sugar metabolism, plant hormone signal transduction, and MAPK signaling. Quantitative proteomics revealed 1,518 differentially accumulated proteins (342 increased and 1,176 decreased in AF), highlighting a global trend toward reduced protein abundance in aborted embryos. Integrated transcriptome-proteome analysis detected 374 shared features with strong concordance between mRNA and protein fold changes (93.6% concordant; r = 0.82), reinforcing a coordinated regulatory program at the abortion stage. Across datasets, embryo abortion was associated with disrupted boron-related cell wall processes, altered carbohydrate transport and mobilization, extensive hormone/MAPK rewiring, and pronounced repression of chloroplast-associated programs including photosynthetic light reactions and pigment/tetrapyrrole metabolism, coupled with redox and energy imbalance. qRT-PCR of eight mechanism-anchored candidates supported RNA-seq trends. Together, these results support a model in which embryonic boron depletion and impaired cell wall integrity are associated with, and may contribute to, a cascade of metabolic and signaling reprogramming that culminates in embryo growth arrest and degeneration, providing actionable markers and targets to improve seed development and fruit set in longan.