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(2016)PLANT PHYSIOLOGY.171(1).p.215-229 Mark abstract In plants, clathrin-mediated endocytosis (CME) is dependent on the function of clathrin and its accessory heterooligomeric adaptor protein complexes, ADAPTOR PROTEIN2 (AP-2) and the TPLATE complex (TPC), and is negatively regulated by the hormones auxin and salicylic acid (SA). The details for how clathrin and its adaptor complexes are recruited to the plasma membrane (PM) to regulate CME, however, are poorly understood. We found that SA and the pharmacological CME inhibitor tyrphostin A23 reduce the membrane association of clathrin and AP-2, but not that of the TPC, whereas auxin solely affected clathrin membrane association, in Arabidopsis (Arabidopsis thaliana). Genetic and pharmacological experiments revealed that loss of AP2 mu or AP2 sigma partially affected the membrane association of other AP-2 subunits and that the AP-2 subunit AP2 sigma, but not AP2 mu, was required for SA-and tyrphostin A23-dependent inhibition of CME. Furthermore, we show that although AP-2 and the TPC are both required for the PM recruitment of clathrin in wild-type cells, the TPC is necessary for clathrin PM association in AP-2-deficient cells. These results indicate that developmental signals may differentially modulate the membrane recruitment of clathrin and its core accessory complexes to regulate the process of CME in plant cells.

Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-7244223



Autor: Chao Wang, Tianwei Hu, Xu Yan, Tingting Meng, Yutong Wang, Qingmei Wang, Xiaoyue Zhang, Ying Gu, Clara Sánchez-Rodríguez, Astrid

Fuente: https://biblio.ugent.be/publication/7244223



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