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

Developmental cell | Jul 24, 2017

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.

Pubmed ID: 28689759 RIS Download

Mesh terms: Actins | Animals | Axon Guidance | Biocatalysis | Biomechanical Phenomena | Cell Adhesion Molecules | Cell Proliferation | Drosophila melanogaster | Humans | Imatinib Mesylate | Intercellular Signaling Peptides and Proteins | Mice, Nude | Mixed Function Oxygenases | Models, Biological | Neoplasms | Nerve Tissue Proteins | Oxidation-Reduction | Phosphorylation | Protein Binding | Protein Domains | Proto-Oncogene Proteins c-abl | Semaphorins | Signal Transduction

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