Defense-growth balance orchestrates bud germination fate in field established sugarcane from a transcriptomic and metabolomic perspective

Bud germination rate and emergence uniformity are critical agronomic traits for sugarcane production, as they directly influence raw cane consumption during planting and the formation of ratooning ability. In this study, we employed integrated transcriptomic and metabolomic analyses to explore the molecular factors that distinguish successful from failed bud germination in field-grown cultivar YZ08–1609 across key developmental stages. Our multi-omics profiling and functional enrichment analysis highlighted critical pathway networks, including carbohydrate metabolism, phytohormone biosynthesis and signaling, plant-pathogen interactions and MAPK cascades ( MEKK1, WRKY24/35 ), and ROS-hormonal crosstalk ( RBOHB, ERF094, ACS6 ). Notably, weighted gene co-expression network analysis (WGCNA) identified two germination-promoting modules enriched with proline-rich protein genes ( TPRP-F1 , PRP4 ), cell wall remodeling factor ( WAT1 ), ethylene biosynthesis genes ( MAO1Bs ), and histone modifiers (Histone H2B.5, etc.), as well as two germination-inhibiting modules dominated by methylation regulator ( OMT3 ), defence-related genes ( Barwin , Zlp ) and flavonoid biosynthetic factors ( CHS1 , ANR ). Further mechanism studies showed that these modules coordinate the growth-defence balance through four interconnected mechanisms: (i) metabolic balance between the production and consumption of ROS, (ii) epigenetic chromatin reorganization via histone modifications, (iii) methylation-driven transcriptional regulation, and (iv) phytoalexin-dependent pathogen resistance. Overall, this study provides the first detailed map of the molecular networks governing sugarcane bud germination. • The growth-defence trade-off determined the success and failure of sugarcane bud germination. • Moderate ROS promoted bud germination, whereas excessive ROS led to germination failure. • Bud germination was coordinately promoted by cell wall remodeling. • Histone modifications facilitated germination through chromatin reorganization. • O-methylation and Barwin-dependent pathogen defence restrained bud germination.