Spatial mapping of juxtacrine axo-glial interactions identifies novel molecules in peripheral myelination

Y. Poitelon, S. Bogni, V. Matafora, G. Della-Flora Nunes, E. Hurley, M. Ghidinelli, Benita S Katzenellenbogen, C. Taveggia, N. Silvestri, A. Bachi, A. Sannino, L. Wrabetz, M. L. Feltri

Research output: Contribution to journalArticle

Abstract

Cell-cell interactions promote juxtacrine signals in specific subcellular domains, which are difficult to capture in the complexity of the nervous system. For example, contact between axons and Schwann cells triggers signals required for radial sorting and myelination. Failure in this interaction causes dysmyelination and axonal degeneration. Despite its importance, few molecules at the axo-glial surface are known. To identify novel molecules in axo-glial interactions, we modified the 'pseudopodia' sub-fractionation system and isolated the projections that glia extend when they receive juxtacrine signals from axons. By proteomics we identified the signalling networks present at the glial-leading edge, and novel proteins, including members of the Prohibitin family. Glial-specific deletion of Prohibitin-2 in mice impairs axo-glial interactions and myelination. We thus validate a novel method to model morphogenesis and juxtacrine signalling, provide insights into the molecular organization of the axo-glial contact, and identify a novel class of molecules in myelination.

Original languageEnglish (US)
Article number8303
JournalNature communications
Volume6
DOIs
StatePublished - Sep 18 2015

Fingerprint

Neuroglia
axons
Molecules
molecules
interactions
nervous system
deletion
degeneration
leading edges
classifying
Axons
cells
fractionation
mice
actuators
projection
Pseudopodia
proteins
Schwann Cells
Neurology

ASJC Scopus subject areas

  • Chemistry(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Physics and Astronomy(all)

Cite this

Poitelon, Y., Bogni, S., Matafora, V., Della-Flora Nunes, G., Hurley, E., Ghidinelli, M., ... Feltri, M. L. (2015). Spatial mapping of juxtacrine axo-glial interactions identifies novel molecules in peripheral myelination. Nature communications, 6, [8303]. https://doi.org/10.1038/ncomms9303

Spatial mapping of juxtacrine axo-glial interactions identifies novel molecules in peripheral myelination. / Poitelon, Y.; Bogni, S.; Matafora, V.; Della-Flora Nunes, G.; Hurley, E.; Ghidinelli, M.; Katzenellenbogen, Benita S; Taveggia, C.; Silvestri, N.; Bachi, A.; Sannino, A.; Wrabetz, L.; Feltri, M. L.

In: Nature communications, Vol. 6, 8303, 18.09.2015.

Research output: Contribution to journalArticle

Poitelon, Y, Bogni, S, Matafora, V, Della-Flora Nunes, G, Hurley, E, Ghidinelli, M, Katzenellenbogen, BS, Taveggia, C, Silvestri, N, Bachi, A, Sannino, A, Wrabetz, L & Feltri, ML 2015, 'Spatial mapping of juxtacrine axo-glial interactions identifies novel molecules in peripheral myelination', Nature communications, vol. 6, 8303. https://doi.org/10.1038/ncomms9303
Poitelon Y, Bogni S, Matafora V, Della-Flora Nunes G, Hurley E, Ghidinelli M et al. Spatial mapping of juxtacrine axo-glial interactions identifies novel molecules in peripheral myelination. Nature communications. 2015 Sep 18;6. 8303. https://doi.org/10.1038/ncomms9303
Poitelon, Y. ; Bogni, S. ; Matafora, V. ; Della-Flora Nunes, G. ; Hurley, E. ; Ghidinelli, M. ; Katzenellenbogen, Benita S ; Taveggia, C. ; Silvestri, N. ; Bachi, A. ; Sannino, A. ; Wrabetz, L. ; Feltri, M. L. / Spatial mapping of juxtacrine axo-glial interactions identifies novel molecules in peripheral myelination. In: Nature communications. 2015 ; Vol. 6.
@article{9919834cb63f4095982108c9f0c83696,
title = "Spatial mapping of juxtacrine axo-glial interactions identifies novel molecules in peripheral myelination",
abstract = "Cell-cell interactions promote juxtacrine signals in specific subcellular domains, which are difficult to capture in the complexity of the nervous system. For example, contact between axons and Schwann cells triggers signals required for radial sorting and myelination. Failure in this interaction causes dysmyelination and axonal degeneration. Despite its importance, few molecules at the axo-glial surface are known. To identify novel molecules in axo-glial interactions, we modified the 'pseudopodia' sub-fractionation system and isolated the projections that glia extend when they receive juxtacrine signals from axons. By proteomics we identified the signalling networks present at the glial-leading edge, and novel proteins, including members of the Prohibitin family. Glial-specific deletion of Prohibitin-2 in mice impairs axo-glial interactions and myelination. We thus validate a novel method to model morphogenesis and juxtacrine signalling, provide insights into the molecular organization of the axo-glial contact, and identify a novel class of molecules in myelination.",
author = "Y. Poitelon and S. Bogni and V. Matafora and {Della-Flora Nunes}, G. and E. Hurley and M. Ghidinelli and Katzenellenbogen, {Benita S} and C. Taveggia and N. Silvestri and A. Bachi and A. Sannino and L. Wrabetz and Feltri, {M. L.}",
year = "2015",
month = "9",
day = "18",
doi = "10.1038/ncomms9303",
language = "English (US)",
volume = "6",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",

}

TY - JOUR

T1 - Spatial mapping of juxtacrine axo-glial interactions identifies novel molecules in peripheral myelination

AU - Poitelon, Y.

AU - Bogni, S.

AU - Matafora, V.

AU - Della-Flora Nunes, G.

AU - Hurley, E.

AU - Ghidinelli, M.

AU - Katzenellenbogen, Benita S

AU - Taveggia, C.

AU - Silvestri, N.

AU - Bachi, A.

AU - Sannino, A.

AU - Wrabetz, L.

AU - Feltri, M. L.

PY - 2015/9/18

Y1 - 2015/9/18

N2 - Cell-cell interactions promote juxtacrine signals in specific subcellular domains, which are difficult to capture in the complexity of the nervous system. For example, contact between axons and Schwann cells triggers signals required for radial sorting and myelination. Failure in this interaction causes dysmyelination and axonal degeneration. Despite its importance, few molecules at the axo-glial surface are known. To identify novel molecules in axo-glial interactions, we modified the 'pseudopodia' sub-fractionation system and isolated the projections that glia extend when they receive juxtacrine signals from axons. By proteomics we identified the signalling networks present at the glial-leading edge, and novel proteins, including members of the Prohibitin family. Glial-specific deletion of Prohibitin-2 in mice impairs axo-glial interactions and myelination. We thus validate a novel method to model morphogenesis and juxtacrine signalling, provide insights into the molecular organization of the axo-glial contact, and identify a novel class of molecules in myelination.

AB - Cell-cell interactions promote juxtacrine signals in specific subcellular domains, which are difficult to capture in the complexity of the nervous system. For example, contact between axons and Schwann cells triggers signals required for radial sorting and myelination. Failure in this interaction causes dysmyelination and axonal degeneration. Despite its importance, few molecules at the axo-glial surface are known. To identify novel molecules in axo-glial interactions, we modified the 'pseudopodia' sub-fractionation system and isolated the projections that glia extend when they receive juxtacrine signals from axons. By proteomics we identified the signalling networks present at the glial-leading edge, and novel proteins, including members of the Prohibitin family. Glial-specific deletion of Prohibitin-2 in mice impairs axo-glial interactions and myelination. We thus validate a novel method to model morphogenesis and juxtacrine signalling, provide insights into the molecular organization of the axo-glial contact, and identify a novel class of molecules in myelination.

UR - http://www.scopus.com/inward/record.url?scp=84942014590&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84942014590&partnerID=8YFLogxK

U2 - 10.1038/ncomms9303

DO - 10.1038/ncomms9303

M3 - Article

VL - 6

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 8303

ER -