Arhgap22 Disruption Leads to RAC1 Hyperactivity Affecting Hippocampal Glutamatergic Synapses and Cognition in Mice.


Journal

Molecular neurobiology
ISSN: 1559-1182
Titre abrégé: Mol Neurobiol
Pays: United States
ID NLM: 8900963

Informations de publication

Date de publication:
Dec 2021
Historique:
received: 07 10 2020
accepted: 15 07 2021
pubmed: 30 8 2021
medline: 18 3 2022
entrez: 29 8 2021
Statut: ppublish

Résumé

Rho GTPases are a class of G-proteins involved in several aspects of cellular biology, including the regulation of actin cytoskeleton. The most studied members of this family are RHOA and RAC1 that act in concert to regulate actin dynamics. Recently, Rho GTPases gained much attention as synaptic regulators in the mammalian central nervous system (CNS). In this context, ARHGAP22 protein has been previously shown to specifically inhibit RAC1 activity thus standing as critical cytoskeleton regulator in cancer cell models; however, whether this function is maintained in neurons in the CNS is unknown. Here, we generated a knockout animal model for arhgap22 and provided evidence of its role in the hippocampus. Specifically, we found that ARHGAP22 absence leads to RAC1 hyperactivity and to an increase in dendritic spine density with defects in synaptic structure, molecular composition, and plasticity. Furthermore, arhgap22 silencing causes impairment in cognition and a reduction in anxiety-like behavior in mice. We also found that inhibiting RAC1 restored synaptic plasticity in ARHGAP22 KO mice. All together, these results shed light on the specific role of ARHGAP22 in hippocampal excitatory synapse formation and function as well as in learning and memory behaviors.

Identifiants

pubmed: 34455539
doi: 10.1007/s12035-021-02502-x
pii: 10.1007/s12035-021-02502-x
pmc: PMC8639580
doi:

Substances chimiques

GTPase-Activating Proteins 0
Neuropeptides 0
Rac1 protein, mouse 0
Glutamic Acid 3KX376GY7L
rac1 GTP-Binding Protein EC 3.6.5.2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

6092-6110

Subventions

Organisme : Fondazione Telethon
ID : GGP17283
Organisme : Ministero della Salute
ID : GR-2016-02361366
Organisme : Regione Lombardia
ID : 227333

Informations de copyright

© 2021. The Author(s).

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Auteurs

Anna Longatti (A)

Institute of Neuroscience, CNR, Milan, 20129, Italy.
Department of Pharmacological and Biomolecular Sciences, Università Degli Studi Di Milano, 20133, Milan, Italy.

Luisa Ponzoni (L)

Institute of Neuroscience, CNR, Milan, 20129, Italy.

Edoardo Moretto (E)

Institute of Neuroscience, CNR, Milan, 20129, Italy.
NeuroMI Milan Center for Neuroscience, Università Milano-Bicocca, 20126, Milan, Italy.

Giorgia Giansante (G)

Institute of Neuroscience, CNR, Milan, 20129, Italy.
NeuroMI Milan Center for Neuroscience, Università Milano-Bicocca, 20126, Milan, Italy.

Norma Lattuada (N)

Department of Medical Biotechnology and Translational Medicine, Università Degli Studi Di Milano, 20129, Milan, Italy.

Maria Nicol Colombo (MN)

Department of Medical Biotechnology and Translational Medicine, Università Degli Studi Di Milano, 20129, Milan, Italy.

Maura Francolini (M)

Department of Medical Biotechnology and Translational Medicine, Università Degli Studi Di Milano, 20129, Milan, Italy.

Mariaelvina Sala (M)

Institute of Neuroscience, CNR, Milan, 20129, Italy.
NeuroMI Milan Center for Neuroscience, Università Milano-Bicocca, 20126, Milan, Italy.

Luca Murru (L)

Institute of Neuroscience, CNR, Milan, 20129, Italy. luca.murru@in.cnr.it.
NeuroMI Milan Center for Neuroscience, Università Milano-Bicocca, 20126, Milan, Italy. luca.murru@in.cnr.it.

Maria Passafaro (M)

Institute of Neuroscience, CNR, Milan, 20129, Italy. maria.passafaro@in.cnr.it.
NeuroMI Milan Center for Neuroscience, Università Milano-Bicocca, 20126, Milan, Italy. maria.passafaro@in.cnr.it.

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