AnkyrinG is required to maintain axo-dendritic polarity in vivo

Sobotzik, Jürgen-Markus, Sie, Jana Maria, Politi, Chrisoula, Del Turco, Domenico, Bennett, Vann, Deller, Thomas, Ghebremedhin, Estifanos and Schultz, Christian (2009). AnkyrinG is required to maintain axo-dendritic polarity in vivo. In: Procceedings of the National Academy of Sciences of the United States of America. Society for Neuroscience 38th Annual meeting, Chicago, IL, U.S.A., (17564-17569). 17-21 October, 2009. doi:10.1073/pnas.0909267106

Author Sobotzik, Jürgen-Markus
Sie, Jana Maria
Politi, Chrisoula
Del Turco, Domenico
Bennett, Vann
Deller, Thomas
Ghebremedhin, Estifanos
Schultz, Christian
Title of paper AnkyrinG is required to maintain axo-dendritic polarity in vivo
Conference name Society for Neuroscience 38th Annual meeting
Conference location Chicago, IL, U.S.A.
Conference dates 17-21 October, 2009
Proceedings title Procceedings of the National Academy of Sciences of the United States of America   Check publisher's open access policy
Journal name Proceedings of the National Academy of Sciences of the United States of America   Check publisher's open access policy
Place of Publication Washington, D.C. U.S.A.
Publisher National Academy of Sciences of the U.S.A
Publication Year 2009
Sub-type Fully published paper
DOI 10.1073/pnas.0909267106
Open Access Status Not Open Access
ISSN 0027-8424
Volume 106
Issue 41
Start page 17564
End page 17569
Total pages 6
Language eng
Abstract/Summary Neurons are highly polarized cells that extend a single axon and several dendrites. Studies with cultured neurons indicate that the proximal portion of the axon, denoted as the axon initial segment (AIS), maintains neuronal polarity in vitro. The membrane-adaptor protein ankyrinG (ankG) is an essential component of the AIS. To determine the relevance of ankG for neuronal polarity in vivo, we studied mice with a cerebellum-specific ankG deficiency. Strikingly, ankG-depleted axons develop protrusions closely resembling dendritic spines. Such axonal spines are enriched with postsynaptic proteins, including ProSAP1/Shank2 and ionotropic and metabotropic glutamate receptors. In addition, immunofluorescence indicated that axonal spines are contacted by presynaptic glutamatergic boutons. For further analysis, double mutants were obtained by crossbreeding ankG−/− mice with L7/Purkinje cell-specific promoter 2 (PCP2) mice expressing enhanced green fluorescent protein (EGFP) in Purkinje cells (PCs). This approach allowed precise confocal microscopic mapping of EGFP-positive spiny axons and their subsequent identification at the electron microscopic level. Ultrastructurally, axonal spines contained a typical postsynaptic density and established asymmetric excitatory synapses with presynaptic boutons containing synaptic vesicles. In the shaft of spiny axons, typical ultrastructural features of the AIS, including the membrane-associated dense undercoating and cytoplasmic bundles of microtubules, were absent. Finally, using time-lapse imaging of organotypic cerebellar slice cultures, we demonstrate that nonspiny PC axons of EGFP-positive/ankG−/− mice acquire a spiny phenotype within a time range of only 3 days. Collectively, these findings demonstrate that axons of ankG-deficient mice acquire hallmark features of dendrites. AnkG thus is important for maintaining appropriate axo-dendritic polarity in vivo.
Keyword Axon initial segment
Axonal differentiation
Diffusion barrier
Q-Index Code E1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Conference Paper
Collection: School of Biomedical Sciences Publications
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Created: Wed, 17 Nov 2010, 16:12:11 EST by Dr Estifanos Ghebremedhin on behalf of School of Biomedical Sciences