Boron Toxicity Modulates Hypocotyl Growth Through Brassinosteroid and Thermomorphogenic-Like Mechanisms.

Abstract

Boron toxicity (BT) is a significant environmental stressor that negatively affects plant development, yet its molecular mechanisms remain poorly understood. Interestingly, certain toxic concentrations of boron trigger hypocotyl elongation, suggesting a complex hormonal response. In this study, we focus on the role of brassinosteroids (BRs) in mediating this atypical growth. Our findings demonstrate that BT stimulates BR biosynthesis while simultaneously suppressing its inactivation, resulting in sustained BR activity throughout seedling development. Furthermore, we provide evidence that BT disrupts the normal BR negative feedback regulation, potentially converting it into a positive feedback mechanism that amplifies the elongation response. We also show that this response shares mechanistic similarities with thermomorphogenesis, particularly in its reliance on COP1, PIF4, and BR signalling pathways. Loss-of-function mutants of COP1 and PIF4 exhibited reduced hypocotyl elongation, underscoring their essential roles in this process. Although further research is needed to fully clarify the molecular details, our work reveals a previously unrecognised connection between BT responses and thermomorphogenic growth. We also propose a working model to better understand how BR signalling contributes to plant adaptation under BT stress conditions.