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Conventional and Non-Conventional Roles of Non-Muscle Myosin II-Actin in Neuronal Development and Degeneration

Institut de Neurociències, Department de Bioquímica i Biologia Molecular, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Universitat Autònoma de Barcelona, 08193 Barcelona, Spain
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Author to whom correspondence should be addressed.
Current affiliation: GIGA Stem Cells, GIGA-Neurosciences, University of Liège, C.H.U. Sart Tilman, 4000 Liège, Belgium.
Cells 2020, 9(9), 1926; https://doi.org/10.3390/cells9091926
Received: 20 July 2020 / Revised: 12 August 2020 / Accepted: 13 August 2020 / Published: 19 August 2020
(This article belongs to the Special Issue Actin-Myosin Cytoskeleton Regulation and Function)
Myosins are motor proteins that use chemical energy to produce mechanical forces driving actin cytoskeletal dynamics. In the brain, the conventional non-muscle myosin II (NMII) regulates actin filament cytoskeletal assembly and contractile forces during structural remodeling of axons and dendrites, contributing to morphology, polarization, and migration of neurons during brain development. NMII isoforms also participate in neurotransmission and synaptic plasticity by driving actin cytoskeletal dynamics during synaptic vesicle release and retrieval, and formation, maturation, and remodeling of dendritic spines. NMIIs are expressed differentially in cerebral non-neuronal cells, such as microglia, astrocytes, and endothelial cells, wherein they play key functions in inflammation, myelination, and repair. Besides major efforts to understand the physiological functions and regulatory mechanisms of NMIIs in the nervous system, their contributions to brain pathologies are still largely unclear. Nonetheless, genetic mutations or deregulation of NMII and its regulatory effectors are linked to autism, schizophrenia, intellectual disability, and neurodegeneration, indicating non-conventional roles of NMIIs in cellular mechanisms underlying neurodevelopmental and neurodegenerative disorders. Here, we summarize the emerging biological roles of NMIIs in the brain, and discuss how actomyosin signaling contributes to dysfunction of neurons and glial cells in the context of neurological disorders. This knowledge is relevant for a deep understanding of NMIIs on the pathogenesis and therapeutics of neuropsychiatric and neurodegenerative diseases. View Full-Text
Keywords: myosin; actin; Rho GTPase; cytoskeletal motors; actomyosin; nucleokinesis; synapse; neuronal polarization; synaptic plasticity; brain injury; neurodegeneration; intellectual disability myosin; actin; Rho GTPase; cytoskeletal motors; actomyosin; nucleokinesis; synapse; neuronal polarization; synaptic plasticity; brain injury; neurodegeneration; intellectual disability
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Javier-Torrent, M.; Saura, C.A. Conventional and Non-Conventional Roles of Non-Muscle Myosin II-Actin in Neuronal Development and Degeneration. Cells 2020, 9, 1926.

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