PIN-FORMED (PIN)-dependent directional auxin transport is crucial for plant development. Although the redistribution of auxin mediated by the polar-ization of PIN3 plays key roles in modulating hy-pocotyl cell expansion, how PIN3 becomes repo-larized to the proper sites within hypocotyl cells is poorly understood. We previously generated the clathrin light chain clc2-1 clc3-1 double mutant in Arabidopsis thaliana and found that it has an elon-gated hypocotyl phenotype compared to the wild type. Here, we performed genetic, cell biology, and pharmacological analyses combined with live-cell imaging to elucidate the molecular mechanism un-derlying the role of clathrin light chains in hypocotyl elongation. Our analyses indicated that the defects of the double mutant enhanced auxin maxima in epidermal cells, thus, promoting hypocotyl elonga-tion. PIN3 relocated to the lateral sides of hypocotyl endodermal cells in clc2-1 clc3-1 mutants to re-direct auxin toward the epidermal cell layers. Moreover, the loss of function of PIN3 largely sup-pressed the long hypocotyl phenotype of the clc2-1 clc3-1 double mutant, as did treatment with auxin transport inhibitors. Based on these data, we pro-pose that clathrin modulates PIN3 abundance and polarity to direct auxin flux and inhibit cell elonga-tion in the hypocotyl, providing novel insights into the regulation of hypocotyl elongation.