A key function for microtubule-associated-protein 6 in activity-dependent stabilisation of actin filaments in dendritic spines

Emerging evidence indicates that microtubule-associated proteins (MAPs) are implicated in synaptic function; in particular, mice deficient for MAP6 exhibit striking deficits in plasticity and cognition. How MAP6 connects to plasticity mechanisms is unclear. Here, we address the possible role of this...

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Authors: Peris, Leticia; Bisbal, Mariano; Martinez Hernandez, José; Saoudi, Yasmina; Jonckheere, Julie; Rolland, Marta; Sebastien, Muriel; Brocard, Jacques; Denarier, Eric; Bosc, Christopher; Guerin, Christophe; Gory Fauré, Sylvie; Deloulme, Jean Christophe; Lanté, Fabien; Arnal, Isabelle; Buisson, Alain; Goldberg, Yves; Blanchoin, Laurent; Delphin, Christian; Andrieux, Annie
Format: Article
Status:Published version
Publication date:2018
Country:Argentina
Institution:Consejo Nacional de Investigaciones Científicas y Técnicas
Repository:CONICET Digital (CONICET)
Language:English
OAI Identifier:oai:ri.conicet.gov.ar:11336/96846
Online Access:http://hdl.handle.net/11336/96846
Access Level:Open access
Keyword:Dendritic Spines
MAP6
Actin
Neurons
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
Summary:Emerging evidence indicates that microtubule-associated proteins (MAPs) are implicated in synaptic function; in particular, mice deficient for MAP6 exhibit striking deficits in plasticity and cognition. How MAP6 connects to plasticity mechanisms is unclear. Here, we address the possible role of this protein in dendritic spines. We find that in MAP6-deficient cortical and hippocampal neurons, maintenance of mature spines is impaired, and can be restored by expressing a stretch of the MAP6 sequence called Mc modules. Mc modules directly bind actin filaments and mediate activity-dependent stabilisation of F-actin in dendritic spines, a key event of synaptic plasticity. In vitro, Mc modules enhance actin filament nucleation and promote the formation of stable, highly ordered filament bundles. Activity-induced phosphorylation of MAP6 likely controls its transfer to the spine cytoskeleton. These results provide a molecular explanation for the role of MAP6 in cognition, enlightening the connection between cytoskeletal dysfunction, synaptic impairment and neuropsychiatric illnesses.

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