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第一作者:Xingyun Qi
第一单位:华盛顿大学
通讯作者:Keiko U Torii
Abstract
背景回顾:Receptor endocytosis is important for signal activation, transduction, and deactivation.
提出问题:However, how a receptor interprets conflicting signals to adjust cellular output is not clearly understood. 主要研究:Using genetic, cell biological, and pharmacological approaches, we report here that ERECTA-LIKE1 (ERL1), the major receptor restricting plant stomatal differentiation, undergoes dynamic subcellular behaviors in response to different EPIDERMAL PATTERNING FACTOR (EPF) peptides. 结果-1:Activation of ERL1 by EPF1 induces rapid ERL1 internalization via multivesicular bodies/late endosomes to vacuolar degradation, whereas ERL1 constitutively internalizes in the absence of EPF1. 结果-2:The co-receptor, TOO MANY MOUTHS is essential for ERL1 internalization induced by EPF1 but not by EPFL6. 结果-3:The peptide antagonist, Stomagen, triggers retention of ERL1 in the endoplasmic reticulum, likely coupled with reduced endocytosis. 结果-4:In contrast, the dominant-negative ERL1 remained dysfunctional in ligand-induced subcellular trafficking. 结论:Our study elucidates that multiple related yet unique peptides specify cell fate by deploying the differential subcellular dynamics of a single receptor.
摘 要
受体内吞对于信号激活、转导和失活都非常重要。但是,目前尚不清楚一个受体如何响应冲突的信号来调整细胞层面的输出。通过遗传学、细胞生物学以及药理学的方法,作者在本文中报道了一个限制植物气孔分化的主要调控受体ERECTA-LIKE1,即ERL1在响应于不同的表皮模式因子EPF多肽时会经历不同的亚细胞动态表现。虽然在不存在EPF1时,ERL1会被组成型的内化,但是由EPF1引起的ERL1激活会通过多囊泡体(multivesicular bodies)或晚期核内体(late endosomes)诱导快速的ERL1内化,到液泡降解。共受体TOO MANY MOUTHS对于由EPF1引起的ERL1内化是必须的,但是不影响由EPFL6引起的ERL1内化。多肽拮抗剂Stomagen所导致的ERL1截留在内质网中很有可能与内吞作用的减少有关。相反,ERL1的显性负性突变会导致配体诱导的亚细胞运输出现功能失调。本文的研究显示,多个相关而又独特的多肽会通过影响单个受体的不同亚细胞动态来指定细胞命运。
通讯作者
**Keiko U Torii** 研究方向: 植物器官发生过程中如何协调增殖与分化。
doi: 10.7554/eLife.58097
Journal: eLife
Published date: Augus 14, 2020
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