Please use this identifier to cite or link to this item: https://hdl.handle.net/10216/110361
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dc.creatorLeite, SC
dc.creatorSampaio, P
dc.creatorSousa, VF
dc.creatorNogueira-Rodrigues, J
dc.creatorPinto-Costa, R
dc.creatorPeters, LL
dc.creatorBrites, P
dc.creatorSousa, MM
dc.date.accessioned2018-01-24T11:25:36Z-
dc.date.available2018-01-24T11:25:36Z-
dc.date.issued2016
dc.identifier.issn2211-1247
dc.identifier.urihttp://hdl.handle.net/10216/110361-
dc.description.abstractThe 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. a-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.
dc.description.sponsorshipWe 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 Premio Melo e Castro - Santa Casa da Misericordia de Lisboa. S.C.L. was supported by Fundacao para a Ciencia e Tecnologia (FCT) (SFRH/BD/72240/2010), and P.B. is an Investigator FCT. Generation of alpha-adducin KO mice was supported by NIH grant HL075714 (to L.L.P.).
dc.language.isoeng
dc.relationinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F72240%2F2010/PT
dc.relation.ispartofCell reports, vol. 15(3), p. 490-498
dc.rightsopenAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAnimals
dc.subjectAxonal Transport
dc.subjectAxons/metabolism
dc.subjectCalmodulin-Binding Proteins/metabolism
dc.subjectCytoskeleton/metabolism
dc.subjectGrowth Cones/metabolism
dc.subjectHippocampus/pathology
dc.subjectMice Inbred C57BL
dc.subjectMice Knockout
dc.subjectMicrofilament Proteins/metabolism
dc.subjectNerve Degeneration/metabolism
dc.subjectNerve Degeneration/pathology
dc.titleThe actin-binding protein α-adducin is required for maintaining axon diameter
dc.typeArtigo em Revista Científica Internacional
dc.contributor.uportoInstituto de Investigação e Inovação em Saúde
dc.identifier.doi10.1016/j.celrep.2016.03.047
dc.relation.publisherversionhttp://www.sciencedirect.com/science/article/pii/S2211124716303187?via%3Dihub
Appears in Collections:I3S - Artigo em Revista Científica Internacional

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