The polarity protein Angiomotin p130 controls dendritic spine maturation

The actin cytoskeleton is essential for the structural changes in dendritic spines that lead to the formation of new synapses. Although the molecular mechanisms underlying spine formation are well characterized, the events that drive spine maturation during development are largely unknown. In this s...

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Bibliographic Details
Published in:The Journal of cell biology 2018-02, Vol.217 (2), p.715-730
Main Authors: Wigerius, Michael, Quinn, Dylan, Diab, Antonios, Clattenburg, Leanne, Kolar, Annette, Qi, Jiansong, Krueger, Stefan R, Fawcett, James P
Format: Article
Language:English
Subjects:
Actin
Animals
Cells, Cultured
Coupling (molecular)
Cytoskeleton
Dendritic spines
Dendritic Spines - metabolism
Dendritic structure
Intercellular Signaling Peptides and Proteins - metabolism
Kinases
Maturation
Membrane Proteins - metabolism
Molecular modelling
Morphogenesis
Neurological diseases
Neurological disorders
Neurons
Phosphorylation
Polarity
Proteins
Rats
Rats, Sprague-Dawley
Spine
Synapses
Synaptogenesis
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Summary:The actin cytoskeleton is essential for the structural changes in dendritic spines that lead to the formation of new synapses. Although the molecular mechanisms underlying spine formation are well characterized, the events that drive spine maturation during development are largely unknown. In this study, we demonstrate that Angiomotin (AMOT-130) is necessary for spine stabilization. AMOT-130 is enriched in mature dendritic spines and functions to stabilize the actin cytoskeleton by coupling F-actin to postsynaptic protein scaffolds. These functions of AMOT are transiently restricted during postnatal development by phosphorylation imposed by the kinase Lats1. Our study proposes that AMOT-130 is essential for normal spine morphogenesis and identifies Lats1 as an upstream regulator in this process. Moreover, our findings may link AMOT-130 loss and the related spine defects to neurological disorders.
ISSN:0021-9525
1540-8140
DOI:10.1083/jcb.201705184