A Thermo‐Sensitive OsMYC2 Allele Coordinates Spikelet Development With Temperature via Proteasome‐Mediated Protein Stability

Elevated temperature disrupts spikelet development and threatens rice yields; however, the underlying molecular mechanisms are not completely elucidated. Although the core jasmonic acid (JA) signalling transcription factor OsMYC2 is essential for spikelet development, it remains unclear whether and how OsMYC2 mediates temperature‐responsive regulation of this process. Here, we identified a thermo‐sensitive panicle defect mutant tspd4 , which exhibits various spikelet abnormalities under high temperature (HT) that are largely reversed under low temperature (LT). Genetic analysis revealed that tspd4 carries a weak allele of OsMYC2 , encoding a protein with a single amino acid deletion (OsMYC2 ΔI128 ). We demonstrated that HT triggers the proteasome‐mediated degradation of OsMYC2 ΔI128 , significantly reducing its abundance. This temperature‐dependent instability impairs the interaction between OsMYC2 ΔI128 and JA signalling repressors (OsJAZs), thereby disrupting downstream transcriptional programmes. We further identified the key floral regulator OsMADS1 as a transcriptional target of OsMYC2 ΔI128 . The OsMADS1 expression is significantly downregulated in tspd4 under HT. Genetic experiments confirm that OsMADS1 functions downstream of OsMYC2 ΔI128 to mediate the thermo‐sensitive spikelet phenotype. Our study uncovers a temperature‐responsive post‐translational mechanism linking a core JA signalling transcription factor to spikelet development in rice, and provides a framework for understanding how ambient temperature reshapes reproductive development through protein stability control.