摘要Cadmium(Cd)toxicity severely limits plant growth and development.Moreover,Cd accu-mulation in vegetables,fruits,and food crops poses health risks to animals and humans.Al-though the root cell wall has been implicated in Cd stress in plants,whether Cd binding by cell wall polysaccharides contributes to tolerance remains controversial,and the mechanism un-derlying transcriptional regulation of cell wall polysaccharide biosynthesis in response to Cd stress is unknown.Here,we functionally char-acterized an Arabidopsis thaliana NAC-type transcription factor,NAC102,revealing its role in Cd stress responses.Cd stress rapidly in-duced accumulation of NAC102.1,the major transcript encoding functional NAC102,espe-cially in the root apex.Compared to wild type(WT)plants,a nac102 mutant exhibited en-hanced Cd sensitivity,whereas NAC102.1-overexpressing plants displayed the opposite phenotype.Furthermore,NAC102 localizes to the nucleus,binds directly to the promoter of WALL-ASSOCIATED KINASE-LIKE PROTEIN11(WAKL11),and induces transcription,thereby facilitating pectin degradation and decreasing Cd binding by pectin.Moreover,WAKL11 over-expression restored Cd tolerance in nac102 mutants to the WT levels,which was correlated with a lower pectin content and lower levels of pectin-bound Cd.Taken together,our work shows that the NAC102-WAKL11 module regu-lates cell wall pectin metabolism and Cd binding,thus conferring Cd tolerance in Arabi-dopsis.