Coconut yield and quality are significantly affected by multiple female inflorescences (MFF), which disrupt flower differentiation balance. To elucidate the molecular mechanisms, we compared MFF with normal female inflorescences (NFF) using phenotypic, morphological, physiological, and multi-omics approaches. The results revealed that MFF exhibited altered flower structures. MFF showed elevated iron (Fe), nitrogen (N), sulfur (S), potassium (K), calcium (Ca), zinc (Zn), proline (Pro), catalase (CAT), malondialdehyde (MDA), abscisic acid (ABA), and jasmonic acid (JA), but reduced molybdenum (Mo), soluble sugar (SS), soluble protein (SP), superoxide dismutase (SOD), peroxidase (POD), indole acetic acid (IAA), zeatin riboside (ZR), and gibberellic acid (GA). We detected 445 differentially expressed genes (DEGs) mainly enriched in ABA, ETH, BR, and JA pathways in MFF compared to NFF. We identified 144 differentially accumulated metabolites (DAMs) primarily in lipids and lipid-like molecules, phenylpropanoids and polyketides, as well as organic acids and derivatives in the comparison of MFF and NFF. Integrated analysis linked these to key pathways, e.g., “carbon metabolism”, “carbon fixation in photosynthetic organisms”, “phenylalanine, tyrosine, and tryptophan biosynthesis”, “glyoxylate and dicarboxylate metabolism”, “glycolysis/gluconeogenesis”, “pentose and glucuronate interconversions”, “flavonoid biosynthesis”, “flavone and flavonol biosynthesis”, “pyruvate metabolism”, and “citrate cycle (TCA cycle)”. Based on our results. the bHLH137, BHLH062, MYB (CSA), ERF118, and MADS2 genes may drive MFF formation. This study provides a framework for understanding coconut flower differentiation and improving yield.

Malformed coconut fruit occurrence exhibits dual impacts on agricultural productivity and economic returns, primarily through substantial yield reduction and compromised commercial value resulting from morphological defects. To elucidate the molecular determinants underlying this developmental anomaly, we conducted a systematic investigation integrating physiological profiling and transcriptomic sequencing on pulp tissues from malformed (MF) and normal (NF) coconut fruits. Notably, MF specimens displayed marked depletion in carbohydrate reserves, with soluble sugars (SS), reducing sugars (RS), starch (SH), soluble proteins (SP), and fat (FA) declining by 28.57%, 20.43%, 15.51%, 36.78%, and 50.18%, respectively, compared to NF controls. Conversely, a coordinated upregulation of phytohormones was observed, where indole acetic acid (IAA), abscisic acid (ABA), cytokinin (CK), gibberellic acid (GA), brassinosteroid (BR), jasmonic acid (JA), and salicylic acid (SA) levels increased by 31.82–92.97%, while ethylene (ETH) exhibited a paradoxical 30.09% reduction. Transcriptomic dissection revealed 6370 functionally annotated differentially expressed genes (DEGs), comprising 4235 upregulated and 2135 downregulated transcripts. These DEGs were predominantly enriched in critical pathways including plant hormone signal transduction, flavonoid/phenylpropanoid biosynthesis, and carbohydrate metabolic networks. Particularly noteworthy was the enhanced activity of cell wall remodeling enzymes—cellulase (CEL), polygalacturonase (PG), and pectinesterase (PE)—accompanied by differential expression of nine cell wall-associated gene families (CEL, PE, PG, PEL, URG, UTR, VTC2, EXP, XET/XTH) and eight phytohormone-related gene clusters. Functional stratification analysis further identified key transcriptional regulators, with MYB, ERF/AP2, BHLH, WRKY, bZIP, and MADS transcription factors demonstrating significant expression divergence, suggesting their pivotal regulatory roles in MF pathogenesis. This multi-omics integration not only deciphers the molecular choreography of coconut fruit malformation but also establishes a novel conceptual framework for developmental disorder research in perennial crops.