Abstract
BACKGROUND: The maize female ear is a key reproductive organ whose morphology directly determines yield. Uniconazole, a gibberellin (GA) biosynthesis inhibitor, is used to regulate ear development and improve yield. However, its mode of action on ear morphogenesis remains incompletely defined. RESULTS: We foliar-applied uniconazole (25 mg L(–1)) at the 12-leaf stage and evaluated ear development using morphology, physiology, and transcriptomics. Uniconazole shortened ear length while significantly increasing ear diameter, cob cross-sectional area, and cob cell-wall thickness. The changes of female ear morphology were accompanied by alterations in hormone (IAA, GA, ABA, ZR) levels and carbohydrate (cellulose, hemicellulose, lignin) profiles. Transcriptome analysis revealed a widespread transcriptional reprogramming. This reprogramming was characterized by the down-regulation of putative growth-restricting receptor kinases (e.g., LRR, PERK) and the concerted up-regulation of master transcriptional regulators (NAC, MYB) of secondary cell-wall biosynthesis. In hormone signaling, the down-regulation of auxin-responsive genes and the up-regulation of DELLA repressors indicated the suppression of both IAA and GA signaling pathways. Concurrently, the phenylpropanoid biosynthesis pathway was strongly activated, aligning with enhanced lignin deposition. CONCLUSIONS: Uniconazole reshapes maize female ears into a shorter length and thicker diameter morphology. This is achieved through a coordinated molecular mechanism involving hormone rebalancing, repression of the GA-DELLA signaling pathway, and activation of the NAC/MYB-mediated secondary cell wall biosynthesis pathway. Our findings provide a mechanistic basis for the targeted use of uniconazole in maize cultivation. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12870-026-08218-1.