Motor neuron synapse and axon defects in a C. elegans alpha-tubulin mutant.

Regulation of microtubule dynamics underlies many fundamental cellular mechanisms including cell division, cell motility, and transport. In neurons, microtubules play key roles in cell migration, axon outgrowth, control of axon and synapse growth, and the regulated transport of vesicles and structur...

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Autores principales:	Renee Baran, Liliana Castelblanco, Garland Tang, Ian Shapiro, Alexandr Goncharov, Yishi Jin
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/de02f4d15308427d9b37e6c9d21dfafd
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spelling	oai:doaj.org-article:de02f4d15308427d9b37e6c9d21dfafd2021-12-02T20:11:55ZMotor neuron synapse and axon defects in a C. elegans alpha-tubulin mutant.1932-620310.1371/journal.pone.0009655https://doaj.org/article/de02f4d15308427d9b37e6c9d21dfafd2010-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20300184/?tool=EBIhttps://doaj.org/toc/1932-6203Regulation of microtubule dynamics underlies many fundamental cellular mechanisms including cell division, cell motility, and transport. In neurons, microtubules play key roles in cell migration, axon outgrowth, control of axon and synapse growth, and the regulated transport of vesicles and structural components of synapses. Loss of synapse and axon integrity and disruption of axon transport characterize many neurodegenerative diseases. Recently, mutations that specifically alter the assembly or stability of microtubules have been found to directly cause neurodevelopmental defects or neurodegeneration in vertebrates. We report here the characterization of a missense mutation in the C-terminal domain of C. elegans alpha-tubulin, tba-1(ju89), that disrupts motor neuron synapse and axon development. Mutant ju89 animals exhibit reduction in the number and size of neuromuscular synapses, altered locomotion, and defects in axon extension. Although null mutations of tba-1 show a nearly wild-type pattern, similar axon outgrowth defects were observed in animals lacking the beta-tubulin TBB-2. Genetic analysis reveals that tba-1(ju89) affects synapse development independent of its role in axon outgrowth. tba-1(ju89) is an altered function allele that most likely perturbs interactions between TBA-1 and specific microtubule-associated proteins that control microtubule dynamics and transport of components needed for synapse and axon growth.Renee BaranLiliana CastelblancoGarland TangIan ShapiroAlexandr GoncharovYishi JinPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 3, p e9655 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Renee Baran Liliana Castelblanco Garland Tang Ian Shapiro Alexandr Goncharov Yishi Jin Motor neuron synapse and axon defects in a C. elegans alpha-tubulin mutant.
description	Regulation of microtubule dynamics underlies many fundamental cellular mechanisms including cell division, cell motility, and transport. In neurons, microtubules play key roles in cell migration, axon outgrowth, control of axon and synapse growth, and the regulated transport of vesicles and structural components of synapses. Loss of synapse and axon integrity and disruption of axon transport characterize many neurodegenerative diseases. Recently, mutations that specifically alter the assembly or stability of microtubules have been found to directly cause neurodevelopmental defects or neurodegeneration in vertebrates. We report here the characterization of a missense mutation in the C-terminal domain of C. elegans alpha-tubulin, tba-1(ju89), that disrupts motor neuron synapse and axon development. Mutant ju89 animals exhibit reduction in the number and size of neuromuscular synapses, altered locomotion, and defects in axon extension. Although null mutations of tba-1 show a nearly wild-type pattern, similar axon outgrowth defects were observed in animals lacking the beta-tubulin TBB-2. Genetic analysis reveals that tba-1(ju89) affects synapse development independent of its role in axon outgrowth. tba-1(ju89) is an altered function allele that most likely perturbs interactions between TBA-1 and specific microtubule-associated proteins that control microtubule dynamics and transport of components needed for synapse and axon growth.
format	article
author	Renee Baran Liliana Castelblanco Garland Tang Ian Shapiro Alexandr Goncharov Yishi Jin
author_facet	Renee Baran Liliana Castelblanco Garland Tang Ian Shapiro Alexandr Goncharov Yishi Jin
author_sort	Renee Baran
title	Motor neuron synapse and axon defects in a C. elegans alpha-tubulin mutant.
title_short	Motor neuron synapse and axon defects in a C. elegans alpha-tubulin mutant.
title_full	Motor neuron synapse and axon defects in a C. elegans alpha-tubulin mutant.
title_fullStr	Motor neuron synapse and axon defects in a C. elegans alpha-tubulin mutant.
title_full_unstemmed	Motor neuron synapse and axon defects in a C. elegans alpha-tubulin mutant.
title_sort	motor neuron synapse and axon defects in a c. elegans alpha-tubulin mutant.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/de02f4d15308427d9b37e6c9d21dfafd
work_keys_str_mv	AT reneebaran motorneuronsynapseandaxondefectsinacelegansalphatubulinmutant AT lilianacastelblanco motorneuronsynapseandaxondefectsinacelegansalphatubulinmutant AT garlandtang motorneuronsynapseandaxondefectsinacelegansalphatubulinmutant AT ianshapiro motorneuronsynapseandaxondefectsinacelegansalphatubulinmutant AT alexandrgoncharov motorneuronsynapseandaxondefectsinacelegansalphatubulinmutant AT yishijin motorneuronsynapseandaxondefectsinacelegansalphatubulinmutant
_version_	1718374914500591616

Motor neuron synapse and axon defects in a C. elegans alpha-tubulin mutant.

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