Differential regulation of clathrin and its adaptor proteins during membrane recruitment for endocytosis
Research output: Contribution to journal › Journal article › Research › peer-review
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 AP2m or AP2s partially affected the membrane association of other AP-2 subunits and that the AP-2 subunit AP2s, but not AP2m, 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.
Original language | English |
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Journal | Plant Physiology |
Volume | 171 |
Issue number | 1 |
Pages (from-to) | 215-229 |
Number of pages | 15 |
ISSN | 0032-0889 |
DOIs | |
Publication status | Published - 2016 |
Externally published | Yes |
Bibliographical note
Publisher Copyright:
© 2016 American Society of Plant Biologists. All rights reserved.
ID: 273071658