In plant cells, clathrin and its adaptor protein complexes at the plasma membrane (PM) and/or trans-Golgi network/early endosome (TGN/EE) regulate clathrin-mediated endocytosis and post-Golgi trafficking, processes crucial for responses to many environmental cues. Studies show that phytohormone auxin differentially regulates clathrin light (CLC) and heavy chain (CHC) recruitment to establish the asymmetric distribution of the auxin efflux carrier PIN-FORMED2 (PIN2), promoting root gravitropic responses. The results showed that the loss-of-function of the TGN/EE component protein ECHIDNA (ECH) in Arabidopsis resulted in defective root gravitropism and impaired PIN2 trafficking. We found that levels of membrane-associated clathrin and its adaptor protein complexes AP-1, AP-2, and the TPLATE complex at the PM and/or TGN/EE were reduced in ech mutants. Furthermore, loss of ECH function disrupted the localization of the auxin receptor TRANSMEMBRANE KINASE1 (TMK1), thereby preventing auxin-induced modulation of CLC and CHC membrane association during root gravitropism. These findings suggest that ECH is crucial for the membrane localization of clathrin and its adaptor complexes, highlighting its critical role in clathrin-mediated trafficking and auxin-responsive regulation.