A hypomorphic mutation in the boron transporter OsBOR1 sensitizes rice panicle development to combined stress of boron deficiency and low temperature

Panicle development is an important constraint on crop productivity, but how it is regulated under boron (B) deficiency and low temperature (LT) conditions remains largely unclear. Here, we identified a rice mutant tspd1 ( temperature-sensitive panicle defect 1 ) that exhibits a severe panicle defect under LT but develops near normally under high temperature (HT). Map-based cloning and genetic analysis demonstrated that tspd1 phenotypes are caused by a T563A mutation in the borate efflux transporter OsBOR1, which reduces its borate-binding affinity and leads to constitutive B deficiency regardless temperatures. Notably, despite this intrinsic B deficiency in tspd1 , the severe panicle defect occurs only under LT, indicating that B deficiency alone is insufficient to trigger the phenotype. Instead, the panicle defect in tspd1 requires a synergy between inherent B deficiency and LT stress. Under this combined stress, tspd1 panicles exhibit excessive reactive oxygen species (ROS) accumulation, oxidative damage, and dysregulation of cell wall-related genes. Together, our findings demonstrate that OsBOR1-mediated B transport is essential for maintaining cellular homeostasis and normal panicle development under low temperature conditions, highlighting the importance of nutrient homeostasis in plant adaptation to temperature fluctuations.