Mechanical coupling between transsynaptic N-cadherin adhesions and actin flow stabilizes dendritic spines.
MBoC. 2015-03-01; 26(5): 859-873
DOI: 10.1091/mbc.E14-06-1086
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1. Mol Biol Cell. 2015 Mar 1;26(5):859-73. doi: 10.1091/mbc.E14-06-1086. Epub 2015
Jan 7.
Mechanical coupling between transsynaptic N-cadherin adhesions and actin flow
stabilizes dendritic spines.
Chazeau A(1), Garcia M(2), Czöndör K(1), Perrais D(1), Tessier B(1), Giannone
G(1), Thoumine O(3).
Author information:
(1)Interdisciplinary Institute for Neuroscience, University of Bordeaux, Unité
Mixte de Recherche 5297, F-33000 Bordeaux, France Interdisciplinary Institute for
Neuroscience, Centre Nationale de la Recherche Scientifique, Unité Mixte de
Recherche 5297, F-33000 Bordeaux, France.
(2)Interdisciplinary Institute for Neuroscience, University of Bordeaux, Unité
Mixte de Recherche 5297, F-33000 Bordeaux, France Interdisciplinary Institute for
Neuroscience, Centre Nationale de la Recherche Scientifique, Unité Mixte de
Recherche 5297, F-33000 Bordeaux, France CYTOO, Minatec, Grenoble, 38054
Grenoble, France.
(3)Interdisciplinary Institute for Neuroscience, University of Bordeaux, Unité
Mixte de Recherche 5297, F-33000 Bordeaux, France Interdisciplinary Institute for
Neuroscience, Centre Nationale de la Recherche Scientifique, Unité Mixte de
Recherche 5297, F-33000 Bordeaux, France .
The morphology of neuronal dendritic spines is a critical indicator of synaptic
function. It is regulated by several factors, including the intracellular
actin/myosin cytoskeleton and transcellular N-cadherin adhesions. To examine the
mechanical relationship between these molecular components, we performed
quantitative live-imaging experiments in primary hippocampal neurons. We found
that actin turnover and structural motility were lower in dendritic spines than
in immature filopodia and increased upon expression of a nonadhesive N-cadherin
mutant, resulting in an inverse relationship between spine motility and actin
enrichment. Furthermore, the pharmacological stimulation of myosin II induced the
rearward motion of actin structures in spines, showing that myosin II exerts
tension on the actin network. Strikingly, the formation of stable, spine-like
structures enriched in actin was induced at contacts between dendritic filopodia
and N-cadherin-coated beads or micropatterns. Finally, computer simulations of
actin dynamics mimicked various experimental conditions, pointing to the actin
flow rate as an important parameter controlling actin enrichment in dendritic
spines. Together these data demonstrate that a clutch-like mechanism between
N-cadherin adhesions and the actin flow underlies the stabilization of dendritic
filopodia into mature spines, a mechanism that may have important implications in
synapse initiation, maturation, and plasticity in the developing brain.
© 2015 Chazeau, Garcia, Czöndör, et al. This article is distributed by The
American Society for Cell Biology under license from the author(s). Two months
after publication it is available to the public under an
Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License
(http://creativecommons.org/licenses/by-nc-sa/3.0).
DOI: 10.1091/mbc.E14-06-1086
PMCID: PMC4342023
PMID: 25568337 [Indexed for MEDLINE]