CEPR2 Deficiency Potentiates ABA-Mediated Mitigation of Heavy Metal Toxicity in Plants

Identifying key genes that regulate plant responses to heavy metals (HMs) is crucial for developing effective strategies to limit HM accumulation. While abscisic acid (ABA) is known to mediate stress responses, the molecular mechanisms linking ABA signaling to HM tolerance are poorly understood. This study revealed CEPR2 as the critical receptor-like kinase that integrates ABA-mediated signaling with HM uptake regulation, a novel role not previously reported. Loss-of-function cepr2 mutants exhibited significantly enhanced biomass (30.3% and 32.2% in shoots, 84.1% and 89.7% in roots) under HM/ABA stress compared to WT and CEPR2 overexpressing lines, alongside higher chlorophyll content and photosynthetic activity. Crucially, ABA-induced suppression of HM accumulation in cepr2 was displayed through downregulation of HM absorption-related genes─FIT, IRT1, FRO2, HMA4, NRAMP6, and BTS genes. Structural equation modeling further established CEPR2 as a central node negatively correlating with ABA content but positively with the HM transporter expression that regulates HM accumulation. The present study provides insights into the molecular mechanism mediated by LRR-RLK in response to HM stress and theoretical support for developing strategies to limit HMs in plants.