Differential regulation of clathrin and its adaptor proteins, AP-2 and the TPLATE complex, during their membrane recruitment in Arabidopsis
详细信息    查看官网全文
摘要
In plants,clathrin-mediated endocytosis(CME) is dependent on the function of clathrin and its accessory heterooligomeric adaptor protein complexes,Adaptor Protein 2(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 are however poorly understood. We found that SA and the pharmacological CME inhibitor tyrphostin A23(Tyr 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 thaliana. Genetic and pharmacological experiments revealed that loss of AP2μ or AP2σ partially affected the membrane association of other AP-2 subunits and that the AP-2 subunit AP2σ,but not AP2μ,was required for SA-and Tyr 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.
In plants,clathrin-mediated endocytosis(CME) is dependent on the function of clathrin and its accessory heterooligomeric adaptor protein complexes,Adaptor Protein 2(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 are however poorly understood. We found that SA and the pharmacological CME inhibitor tyrphostin A23(Tyr 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 thaliana. Genetic and pharmacological experiments revealed that loss of AP2μ or AP2σ partially affected the membrane association of other AP-2 subunits and that the AP-2 subunit AP2σ,but not AP2μ,was required for SA-and Tyr 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.
引文

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700