Differential regulation of clathrin and its adaptor proteins during membrane recruitment for endocytosis

Chao Wang, Tianwei Hu, Xu Yan, Tingting Meng, Yutong Wang, Qingmei Wang, Xiaoyue Zhang, Ying Gu, Clara Sánchez-Rodríguez, Astrid Gadeyne, Jinxing Lin, Staffan Persson, Daniël van Damme, Chuanyou Li, Sebastian Y. Bednarek, Jianwei Pan

Research output: Contribution to journalArticle

19 Citations (Scopus)

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 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 languageEnglish (US)
Pages (from-to)215-229
Number of pages15
JournalPlant physiology
Volume171
Issue number1
DOIs
StatePublished - May 1 2016

Fingerprint

Vesicular Transport Adaptor Proteins
clathrin
Clathrin
endocytosis
Endocytosis
membrane proteins
Membrane Proteins
Salicylic Acid
salicylic acid
Indoleacetic Acids
Membranes
Cell Membrane
plasma membrane
Arabidopsis
auxins
Pharmacology
Plant Cells
cells

All Science Journal Classification (ASJC) codes

  • Physiology
  • Genetics
  • Plant Science

Cite this

Wang, Chao ; Hu, Tianwei ; Yan, Xu ; Meng, Tingting ; Wang, Yutong ; Wang, Qingmei ; Zhang, Xiaoyue ; Gu, Ying ; Sánchez-Rodríguez, Clara ; Gadeyne, Astrid ; Lin, Jinxing ; Persson, Staffan ; van Damme, Daniël ; Li, Chuanyou ; Bednarek, Sebastian Y. ; Pan, Jianwei. / Differential regulation of clathrin and its adaptor proteins during membrane recruitment for endocytosis. In: Plant physiology. 2016 ; Vol. 171, No. 1. pp. 215-229.
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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 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.",
author = "Chao Wang and Tianwei Hu and Xu Yan and Tingting Meng and Yutong Wang and Qingmei Wang and Xiaoyue Zhang and Ying Gu and Clara S{\'a}nchez-Rodr{\'i}guez and Astrid Gadeyne and Jinxing Lin and Staffan Persson and {van Damme}, Dani{\"e}l and Chuanyou Li and Bednarek, {Sebastian Y.} and Jianwei Pan",
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Wang, C, Hu, T, Yan, X, Meng, T, Wang, Y, Wang, Q, Zhang, X, Gu, Y, Sánchez-Rodríguez, C, Gadeyne, A, Lin, J, Persson, S, van Damme, D, Li, C, Bednarek, SY & Pan, J 2016, 'Differential regulation of clathrin and its adaptor proteins during membrane recruitment for endocytosis', Plant physiology, vol. 171, no. 1, pp. 215-229. https://doi.org/10.1104/pp.15.01716

Differential regulation of clathrin and its adaptor proteins during membrane recruitment for endocytosis. / Wang, Chao; Hu, Tianwei; Yan, Xu; Meng, Tingting; Wang, Yutong; Wang, Qingmei; Zhang, Xiaoyue; Gu, Ying; Sánchez-Rodríguez, Clara; Gadeyne, Astrid; Lin, Jinxing; Persson, Staffan; van Damme, Daniël; Li, Chuanyou; Bednarek, Sebastian Y.; Pan, Jianwei.

In: Plant physiology, Vol. 171, No. 1, 01.05.2016, p. 215-229.

Research output: Contribution to journalArticle

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T1 - Differential regulation of clathrin and its adaptor proteins during membrane recruitment for endocytosis

AU - Wang, Chao

AU - Hu, Tianwei

AU - Yan, Xu

AU - Meng, Tingting

AU - Wang, Yutong

AU - Wang, Qingmei

AU - Zhang, Xiaoyue

AU - Gu, Ying

AU - Sánchez-Rodríguez, Clara

AU - Gadeyne, Astrid

AU - Lin, Jinxing

AU - Persson, Staffan

AU - van Damme, Daniël

AU - Li, Chuanyou

AU - Bednarek, Sebastian Y.

AU - Pan, Jianwei

PY - 2016/5/1

Y1 - 2016/5/1

N2 - 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.

AB - 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.

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