Oligodendroglial Modulation of Fast Axonal Transport in a Mouse Model of Hereditary Spastic Paraplegia

Oligodendrocytes are critical for the development of the plasma membrane and cytoskeleton of the axon. In this paper, we show that fast axonal transport is also dependent on the oligodendrocyte. Using a mouse model of hereditary spastic paraplegia type 2 due to a null mutation of the myelin Plp gene...

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Veröffentlicht in:The Journal of cell biology 2004-07, Vol.166 (1), p.121-131
Hauptverfasser: Edgar, Julia M., McLaughlin, Mark, Yool, Donald, Zhang, Su-Chun, Fowler, Jill H., Montague, Paul, Barrie, Jennifer A., McCulloch, Mailis C., Duncan, Ian D., Garbern, James, Nave, Klaus A., Griffiths, Ian R.
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container_end_page 131
container_issue 1
container_start_page 121
container_title The Journal of cell biology
container_volume 166
creator Edgar, Julia M.
McLaughlin, Mark
Yool, Donald
Zhang, Su-Chun
Fowler, Jill H.
Montague, Paul
Barrie, Jennifer A.
McCulloch, Mailis C.
Duncan, Ian D.
Garbern, James
Nave, Klaus A.
Griffiths, Ian R.
description Oligodendrocytes are critical for the development of the plasma membrane and cytoskeleton of the axon. In this paper, we show that fast axonal transport is also dependent on the oligodendrocyte. Using a mouse model of hereditary spastic paraplegia type 2 due to a null mutation of the myelin Plp gene, we find a progressive impairment in fast retrograde and anterograde transport. Increased levels of retrograde motor protein subunits are associated with accumulation of membranous organelles distal to nodal complexes. Using cell transplantation, we show categorically that the axonal phenotype is related to the presence of the overlying Plp null myelin. Our data demonstrate a novel role for oligodendrocytes in the local regulation of axonal function and have implications for the axonal loss associated with secondary progressive multiple sclerosis.
doi_str_mv 10.1083/jcb.200312012
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In this paper, we show that fast axonal transport is also dependent on the oligodendrocyte. Using a mouse model of hereditary spastic paraplegia type 2 due to a null mutation of the myelin Plp gene, we find a progressive impairment in fast retrograde and anterograde transport. Increased levels of retrograde motor protein subunits are associated with accumulation of membranous organelles distal to nodal complexes. Using cell transplantation, we show categorically that the axonal phenotype is related to the presence of the overlying Plp null myelin. 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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Alleles
Animals
Axons
Axons - metabolism
Biological Transport
Blotting, Western
Cell Membrane - metabolism
Cellular biology
Cytoskeleton - metabolism
Disease Models, Animal
Heredity
Heterozygote
Immunohistochemistry
Mice
Mice, Mutant Strains
Myelin
Myelin Sheath - metabolism
Nerves
Neurons
Oligodendroglia
Oligodendroglia - metabolism
Optic nerve
Optic Nerve - metabolism
Optics
Organelles
Paralysis
Phenotype
Reverse Transcriptase Polymerase Chain Reaction
Rodents
Spastic Paraplegia, Hereditary - genetics
Spastic Paraplegia, Hereditary - metabolism
Spastic Paraplegia, Hereditary - pathology
Spinal cord
Spinal Cord - pathology
Time Factors
title Oligodendroglial Modulation of Fast Axonal Transport in a Mouse Model of Hereditary Spastic Paraplegia
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