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Cell ReportsVolume 15, Issue 3, 19 April 2016, Pages 490-498

The Actin-Binding Protein α-Adducin Is Required for Maintaining Axon Diameter(Article)(Open Access)

  • aNerve Regeneration Group, IBMC-Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, 4150-180, Portugal
  • bAdvanced Light Microscopy Unit, IBMC-Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, 4150-180, Portugal
  • cInstituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, 4200-135, Portugal
  • dICBAS, Universidade do Porto, Porto, 4050-313, Portugal
  • eThe Jackson Laboratory, Bar Harbor, ME 04609, United States

Abstract

The actin-binding protein adducin was recently identified as a component of the neuronal subcortical cytoskeleton. Here, we analyzed mice lacking adducin to uncover the function of this protein in actin rings. α-adducin knockout mice presented progressive axon enlargement in the spinal cord and optic and sciatic nerves, followed by axon degeneration and loss. Using stimulated emission depletion super-resolution microscopy, we show that a periodic subcortical actin cytoskeleton is assembled in every neuron type inspected including retinal ganglion cells and dorsal root ganglia neurons. In neurons devoid of adducin, the actin ring diameter increased, although the inter-ring periodicity was maintained. In vitro, the actin ring diameter adjusted as axons grew, suggesting the lattice is dynamic. Our data support a model in which adducin activity is not essential for actin ring assembly and periodicity but is necessary to control the diameter of both actin rings and axons and actin filament growth within rings. © 2016 The Authors.

Indexed keywords

EMTREE drug terms:alpha adducinactin binding proteinadducincalmodulin binding protein
EMTREE medical terms:actin filamentanimal cellanimal tissueArticlecell sizecontrolled studygrowth conemousenerve fibernerve fiber transportnonhumanoptic nervepriority journalprotein depletionretina ganglion cellsciatic nervespinal cordanimalaxonC57BL mousecytoskeletonhippocampusknockout mousemetabolismnerve degenerationpathology
MeSH:AnimalsAxonal TransportAxonsCalmodulin-Binding ProteinsCytoskeletonGrowth ConesHippocampusMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsNerve Degeneration

Chemicals and CAS Registry Numbers:

adducin; Calmodulin-Binding Proteins; Microfilament Proteins

Funding details

Funding sponsor Funding number Acronym
Fundação para a Ciência e a Tecnologia
See opportunities		SFRH/BD/72240/2010
National Institutes of Health
See opportunities		HL075714
International Foundation for Research in Paraplegia
See opportunities

  • 1

    We thank the technical support of the IBMC Animal Facility. We are indebted to Leica Microsystems, especially to Dr. Ulf Schwarz, for making a STED microscope available. We thank Dr. Ana Carvalho (IBMC) for fruitful discussions. We thank Dr. Ana Seixas (IBMC) for revising the final version of the manuscript. This work was funded by the International Foundation for Research in Paraplegia (IRP) and by Prémio Melo e Castro - Santa Casa da Misericórdia de Lisboa. S.C.L. was supported by Fundação para a Ciência e Tecnologia (FCT) (SFRH/BD/72240/2010), and P.B. is an Investigator FCT. Generation of α-adducin KO mice was supported by NIH grant HL075714 (to L.L.P.).

  • ISSN: 22111247
  • Source Type: Journal
  • Original language: English
  • DOI: 10.1016/j.celrep.2016.03.047
  • PubMed ID: 27068466
  • Document Type: Article
  • Publisher: Elsevier B.V.

  Sousa, M.M.; Nerve Regeneration Group, IBMC-Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal;
© Copyright 2017 Elsevier B.V., All rights reserved.

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