Slow axoplasmic transport under scrutiny

The origin of axoplasmic proteins is central for the biology of axons. For over fifty years axons have been considered unable to synthesize proteins and that cell bodies supply them with proteins by a slow transport mechanism. To allow for prolonged transport times, proteins were assumed to be stabl...

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Autores principales:	Court,Felipe A, Álvarez,Jaime
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2011
Materias:	Protein synthesis radioactive wave maintenance of axons Schwann cell glia transgenic mouse
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602011000400001
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spelling	oai:scielo:S0716-976020110004000012012-02-10Slow axoplasmic transport under scrutinyCourt,Felipe AÁlvarez,Jaime Protein synthesis radioactive wave maintenance of axons Schwann cell glia transgenic mouse The origin of axoplasmic proteins is central for the biology of axons. For over fifty years axons have been considered unable to synthesize proteins and that cell bodies supply them with proteins by a slow transport mechanism. To allow for prolonged transport times, proteins were assumed to be stable, i.e., not degraded in axons. These are now textbook notions that configure the slow transport model (STM). The aim of this article is to cast doubts on the validity of STM, as a step toward gaining more understanding about the supply of axoplasmic proteins. First, the stability of axonal proteins claimed by STM has been disproved by experimental evidence. Moreover, the evidence for protein synthesis in axons indicates that the repertoire is extensive and the amount sizeable, which disproves the notion that axons are unable to synthesize proteins and that cell bodies supply most axonal proteins. In turn, axoplasmic protein synthesis gives rise to the metabolic model (MM). We point out a few inconsistencies in STM that MM redresses. Although both models address the supply of proteins to axons, so far they have had no crosstalk. Since proteins underlie every conceivable cellular function, it is necessary to re-evaluate in-depth the origin of axonal proteins. We hope this will shape a novel understanding of the biology of axons, with impact on development and maintenance of axons, nerve repair, axonopathies and plasticity, to mention a few fields.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.44 n.4 20112011-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602011000400001en10.4067/S0716-97602011000400001
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	Protein synthesis radioactive wave maintenance of axons Schwann cell glia transgenic mouse
spellingShingle	Protein synthesis radioactive wave maintenance of axons Schwann cell glia transgenic mouse Court,Felipe A Álvarez,Jaime Slow axoplasmic transport under scrutiny
description	The origin of axoplasmic proteins is central for the biology of axons. For over fifty years axons have been considered unable to synthesize proteins and that cell bodies supply them with proteins by a slow transport mechanism. To allow for prolonged transport times, proteins were assumed to be stable, i.e., not degraded in axons. These are now textbook notions that configure the slow transport model (STM). The aim of this article is to cast doubts on the validity of STM, as a step toward gaining more understanding about the supply of axoplasmic proteins. First, the stability of axonal proteins claimed by STM has been disproved by experimental evidence. Moreover, the evidence for protein synthesis in axons indicates that the repertoire is extensive and the amount sizeable, which disproves the notion that axons are unable to synthesize proteins and that cell bodies supply most axonal proteins. In turn, axoplasmic protein synthesis gives rise to the metabolic model (MM). We point out a few inconsistencies in STM that MM redresses. Although both models address the supply of proteins to axons, so far they have had no crosstalk. Since proteins underlie every conceivable cellular function, it is necessary to re-evaluate in-depth the origin of axonal proteins. We hope this will shape a novel understanding of the biology of axons, with impact on development and maintenance of axons, nerve repair, axonopathies and plasticity, to mention a few fields.
author	Court,Felipe A Álvarez,Jaime
author_facet	Court,Felipe A Álvarez,Jaime
author_sort	Court,Felipe A
title	Slow axoplasmic transport under scrutiny
title_short	Slow axoplasmic transport under scrutiny
title_full	Slow axoplasmic transport under scrutiny
title_fullStr	Slow axoplasmic transport under scrutiny
title_full_unstemmed	Slow axoplasmic transport under scrutiny
title_sort	slow axoplasmic transport under scrutiny
publisher	Sociedad de Biología de Chile
publishDate	2011
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602011000400001
work_keys_str_mv	AT courtfelipea slowaxoplasmictransportunderscrutiny AT alvarezjaime slowaxoplasmictransportunderscrutiny
_version_	1718441479620263936

Slow axoplasmic transport under scrutiny

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