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LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons

Neurons extend long processes known as axons and dendrites, through which they communicate with each other. The neuronal circuits formed by the axons and dendrites are the structural basis of higher brain functions. The formation and maintenance of these processes are essential for physiological bra...

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Autores principales: Hisanaga, Shin-ichi, Wei, Ran, Huo, Anni, Tomomura, Mineko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7344150/
https://www.ncbi.nlm.nih.gov/pubmed/32714146
http://dx.doi.org/10.3389/fnmol.2020.00112
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author Hisanaga, Shin-ichi
Wei, Ran
Huo, Anni
Tomomura, Mineko
author_facet Hisanaga, Shin-ichi
Wei, Ran
Huo, Anni
Tomomura, Mineko
author_sort Hisanaga, Shin-ichi
collection PubMed
description Neurons extend long processes known as axons and dendrites, through which they communicate with each other. The neuronal circuits formed by the axons and dendrites are the structural basis of higher brain functions. The formation and maintenance of these processes are essential for physiological brain activities. Membrane components, both lipids, and proteins, that are required for process formation are supplied by vesicle transport. Intracellular membrane trafficking is regulated by a family of Rab small GTPases. A group of Rabs regulating endosomal trafficking has been studied mainly in nonpolarized culture cell lines, and little is known about their regulation in polarized neurons with long processes. As shown in our recent study, lemur tail (former tyrosine) kinase 1 (LMTK1), an as yet uncharacterized Ser/Thr kinase associated with Rab11-positive recycling endosomes, modulates the formation of axons, dendrites, and spines in cultured primary neurons. LMTK1 knockdown or knockout (KO) or the expression of a kinase-negative mutant stimulates the transport of endosomal vesicles in neurons, leading to the overgrowth of axons, dendrites, and spines. More recently, we found that LMTK1 regulates TBC1D9B Rab11 GAP and proposed the Cdk5/p35-LMTK1-TBC1D9B-Rab11 pathway as a signaling cascade that regulates endosomal trafficking. Here, we summarize the biochemical, cell biological, and physiological properties of LMTK1.
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spelling pubmed-73441502020-07-25 LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons Hisanaga, Shin-ichi Wei, Ran Huo, Anni Tomomura, Mineko Front Mol Neurosci Neuroscience Neurons extend long processes known as axons and dendrites, through which they communicate with each other. The neuronal circuits formed by the axons and dendrites are the structural basis of higher brain functions. The formation and maintenance of these processes are essential for physiological brain activities. Membrane components, both lipids, and proteins, that are required for process formation are supplied by vesicle transport. Intracellular membrane trafficking is regulated by a family of Rab small GTPases. A group of Rabs regulating endosomal trafficking has been studied mainly in nonpolarized culture cell lines, and little is known about their regulation in polarized neurons with long processes. As shown in our recent study, lemur tail (former tyrosine) kinase 1 (LMTK1), an as yet uncharacterized Ser/Thr kinase associated with Rab11-positive recycling endosomes, modulates the formation of axons, dendrites, and spines in cultured primary neurons. LMTK1 knockdown or knockout (KO) or the expression of a kinase-negative mutant stimulates the transport of endosomal vesicles in neurons, leading to the overgrowth of axons, dendrites, and spines. More recently, we found that LMTK1 regulates TBC1D9B Rab11 GAP and proposed the Cdk5/p35-LMTK1-TBC1D9B-Rab11 pathway as a signaling cascade that regulates endosomal trafficking. Here, we summarize the biochemical, cell biological, and physiological properties of LMTK1. Frontiers Media S.A. 2020-06-30 /pmc/articles/PMC7344150/ /pubmed/32714146 http://dx.doi.org/10.3389/fnmol.2020.00112 Text en Copyright © 2020 Hisanaga, Wei, Huo and Tomomura. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Hisanaga, Shin-ichi
Wei, Ran
Huo, Anni
Tomomura, Mineko
LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons
title LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons
title_full LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons
title_fullStr LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons
title_full_unstemmed LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons
title_short LMTK1, a Novel Modulator of Endosomal Trafficking in Neurons
title_sort lmtk1, a novel modulator of endosomal trafficking in neurons
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7344150/
https://www.ncbi.nlm.nih.gov/pubmed/32714146
http://dx.doi.org/10.3389/fnmol.2020.00112
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