The Clathrin Adaptor Complex AP-2 Mediates Endocytosis of BRASSINOSTEROID INSENSITIVE1 in Arabidopsis

作者：Simone Di Rubbo, Niloufer G. Irani, Soo Youn Kim, Zheng‐Yi Xu, Astrid Gadeyne, Wim Dejonghe, Isabelle Vanhoutte, Geert Persiau, Dominique Eeckhout, Sibu Simon, Kyungyoung Song, Jürgen Kleine‐Vehn, Jiřı́ Friml, Geert De Jaeger, Daniël Van Damme, Inhwan Hwang, Eugenia Russinova · 发表于：The Plant Cell · 年份：2013 · DOI：10.1105/tpc.113.114058 · 被引用次数：199 · 研究领域：Cellular transport and secretion、Plant Molecular Biology Research、Plant Reproductive Biology

Clathrin-mediated endocytosis (CME) regulates many aspects of plant development, including hormone signaling and responses to environmental stresses. Despite the importance of this process, the machinery that regulates CME in plants is largely unknown. In mammals, the heterotetrameric adaptor protein complex-2 (AP-2) is required for the formation of clathrin-coated vesicles at the plasma membrane (PM). Although the existence of AP-2 has been predicted in Arabidopsis thaliana, the biochemistry and functionality of the complex is still uncharacterized. Here, we identified all the subunits of the Arabidopsis AP-2 by tandem affinity purification and found that one of the large AP-2 subunits, AP2A1, localized at the PM and interacted with clathrin. Furthermore, endocytosis of the leucine-rich repeat receptor kinase, brassinosteroid insensitive1 (BRI1), was shown to depend on AP-2. Knockdown of the two Arabidopsis AP2A genes or overexpression of a dominant-negative version of the medium AP-2 subunit, AP2M, impaired BRI1 endocytosis and enhanced the brassinosteroid signaling. Our data reveal that the CME machinery in Arabidopsis is evolutionarily conserved and that AP-2 functions in receptor-mediated endocytosis.