Transcription factor ANAC087 coordinates symplastic Cd exclusion and apoplastic Cd sequestration to enhance cadmium resistance in Arabidopsis thaliana

Cadmium (Cd) exclusion and sequestration are vital mechanisms for plant survival under heavy metal stress, yet the upstream regulatory networks governing these coordinated processes remain poorly understood. In this study, we identified the NAC transcription factor ANAC087 as a key positive regulator of Cd resistance in Arabidopsis thaliana. Loss-of-function anac087 mutants exhibited hypersensitivity to Cd stress and significantly higher Cd accumulation in both roots and shoots compared to the wild type (WT) Col-0. Mechanistically, we demonstrate that ANAC087 coordinates two complementary pathways involving symplastic Cd influx control and apoplastic sequestration. First, ANAC087 contributes to ABA homeostasis and directly binds to the promoter of ABSCISIC ACID-INSENSITIVE5 (ABI5) to activate its expression, which subsequently antagonizes the MYB49-bHLH38/101 regulatory module to suppress IRT1, thereby limiting Cd uptake. Exogenous ABA application partially alleviated the Cd-sensitive phenotype of anac087. Second, ANAC087 directly transactivates ANAC017 to promote XTH31-mediated xyloglucan accumulation, substantially enhancing the Cd binding capacity of the root cell wall. Genetic analyses confirmed that ectopic expression of ABI5 or ANAC017 partially rescued the Cd sensitive and high-Cd accumulation phenotypes of anac087, whereas XTH31 overexpression complemented the anac017 anac087 double mutant. Furthermore, Cd stress increases both ANAC087 transcript abundance and protein stability. Collectively, our findings support a regulatory framework in which ANAC087 coordinates processes that limit symplastic Cd accumulation and promote apoplastic Cd sequestration.