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首页> 外文期刊>Biology Open >Actin cytoskeleton remodeling defines a distinct cellular function for adhesion G protein-coupled receptors ADGRL/latrophilins 1, 2 and 3
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Actin cytoskeleton remodeling defines a distinct cellular function for adhesion G protein-coupled receptors ADGRL/latrophilins 1, 2 and 3

机译：肌动蛋白细胞骨架重塑为粘附G蛋白偶联受体ADGRL / latrophilins 1、2和3定义了独特的细胞功能

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Latrophilins represent a subgroup of the adhesion G protein-coupled receptor family, which bind to actin-associated scaffolding proteins. They are expressed in various tissues, suggesting that they might participate in biological processes that are ubiquitous. Here we focus on actin cytoskeleton dynamics to explore the role of latrophilins in mammalian cells. Individual overexpression of each latrophilin isoform comparably increased cell volume while modifying the net profile of F-actin-dependent cell extensions, as evaluated by confocal microscopy analysis. Latrophilin deletion mutants evidenced that direct coupling to the intracellular machinery was a requirement for modulating cell extensions. The association between latrophilins and the actin cytoskeleton was detected by co-immunoprecipitation assays and corroborated with immunocytochemistry analysis. Consistent with the destabilization of F-actin structures, latrophilin isoforms constitutively induced a prominent increase in the activity of actin-depolymerizing factor, cofilin. Intercellular adhesion events stabilized by heterophilic Teneurin-4 trans-interactions disrupted latrophilin colocalization with F-actin and led to an isoform-specific rescue of cell extensions. Thus, we find that the actin cytoskeleton machinery constitutes an important component of constitutive as well as ligand-induced signaling for latrophilins.This article has an associated First Person interview with the first author of the paper.
机译：亲脂蛋白代表粘附G蛋白偶联受体家族的一个亚组，与肌动蛋白相关的支架蛋白结合。它们在各种组织中表达，表明它们可能参与了普遍存在的生物过程。在这里，我们专注于肌动蛋白的细胞骨架动力学，以探索乳脂蛋白在哺乳动物细胞中的作用。通过共聚焦显微镜分析评估，每个过氧化物酶同工型的个体过表达相对地增加了细胞体积，同时改变了F-肌动蛋白依赖性细胞延伸的净分布。亲油蛋白缺失突变体证明直接偶联至细胞内机制是调节细胞延伸的必要条件。通过共免疫沉淀测定法检测了亲脂蛋白和肌动蛋白细胞骨架之间的关联，并通过免疫细胞化学分析得到了证实。与F-肌动蛋白结构的失稳相一致，亲脂蛋白同工型组成性地诱导肌动蛋白解聚因子cofilin的活性显着增加。异源Teneurin-4反式相互作用稳定的细胞间粘附事件破坏了Latrophilin与F-actin的共定位，并导致细胞延伸的同种型特异性拯救。因此，我们发现肌动蛋白的细胞骨架机制是组成型以及配体诱导的亲脂蛋白信号传导的重要组成部分。本文与第一作者相关的第一人称访谈。

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