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生长因子信号传导对F-肌动蛋白解聚和细胞排斥的放大作用。

Amplification of F-Actin Disassembly and Cellular Repulsion by Growth Factor Signaling.

作者信息

Yoon Jimok, Kim Sang Bum, Ahmed Giasuddin, Shay Jerry W, Terman Jonathan R

机构信息

Departments of Neuroscience and Pharmacology, Harold C. Simmons Comprehensive Cancer Center, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

Department of Cell Biology, Harold C. Simmons Comprehensive Cancer Center, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

出版信息

Dev Cell. 2017 Jul 24;42(2):117-129.e8. doi: 10.1016/j.devcel.2017.06.007. Epub 2017 Jul 6.

DOI:10.1016/j.devcel.2017.06.007
PMID:28689759
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5564210/
Abstract

Extracellular cues that regulate cellular shape, motility, and navigation are generally classified as growth promoting (i.e., growth factors/chemoattractants and attractive guidance cues) or growth preventing (i.e., repellents and inhibitors). Yet, these designations are often based on complex assays and undefined signaling pathways and thus may misrepresent direct roles of specific cues. Here, we find that a recognized growth-promoting signaling pathway amplifies the F-actin disassembly and repulsive effects of a growth-preventing pathway. Focusing on Semaphorin/Plexin repulsion, we identified an interaction between the F-actin-disassembly enzyme Mical and the Abl tyrosine kinase. Biochemical assays revealed Abl phosphorylates Mical to directly amplify Mical Redox-mediated F-actin disassembly. Genetic assays revealed that Abl allows growth factors and Semaphorin/Plexin repellents to combinatorially increase Mical-mediated F-actin disassembly, cellular remodeling, and repulsive axon guidance. Similar roles for Mical in growth factor/Abl-related cancer cell behaviors further revealed contexts in which characterized positive effectors of growth/guidance stimulate such negative cellular effects as F-actin disassembly/repulsion.

摘要

调节细胞形状、运动性和导航的细胞外信号通常分为促进生长的信号（即生长因子/化学引诱剂和吸引性导向信号）或抑制生长的信号（即排斥剂和抑制剂）。然而，这些分类通常基于复杂的检测方法和不明确的信号通路，因此可能会错误地呈现特定信号的直接作用。在这里，我们发现一个公认的促进生长的信号通路会放大一个抑制生长的信号通路对F-肌动蛋白的解聚作用和排斥作用。聚焦于信号素/丛状蛋白介导的排斥作用，我们确定了F-肌动蛋白解聚酶Mical与Abl酪氨酸激酶之间的相互作用。生化分析表明，Abl使Mical磷酸化，直接放大Mical氧化还原介导的F-肌动蛋白解聚。遗传学分析表明，Abl使生长因子和信号素/丛状蛋白排斥剂共同作用，增加Mical介导的F-肌动蛋白解聚、细胞重塑和轴突排斥导向。Mical在生长因子/Abl相关癌细胞行为中发挥类似作用，进一步揭示了生长/导向的特定正向效应器刺激F-肌动蛋白解聚/排斥等负向细胞效应的情况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4e6/5564210/ca799f4ca35b/nihms883381f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4e6/5564210/ca799f4ca35b/nihms883381f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4e6/5564210/d9f332588c7c/nihms883381f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4e6/5564210/e41811070203/nihms883381f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4e6/5564210/b744a6f726ab/nihms883381f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4e6/5564210/b8995521834a/nihms883381f4.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4e6/5564210/ca799f4ca35b/nihms883381f7.jpg

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MICAL介导的肌动蛋白氧化及其对细胞骨架和细胞动力学的影响。
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