The Noonan syndrome-associated D61G variant of the protein tyrosine phosphatase SHP2 prevents synaptic down-scaling.

SHP2 Src homology 2 domain (SH2 domain) phosphatase phosphorylation phosphotyrosine signaling postsynaptic density protein 95 (PSD95) protein tyrosine phosphatase non-receptor type 11 (PTPN11) synaptic scaling α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA receptor)

Journal

The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R

Informations de publication

Date de publication:
17 07 2020
Historique:
received: 23 07 2019
revised: 01 06 2020
pubmed: 6 6 2020
medline: 15 1 2021
entrez: 6 6 2020
Statut: ppublish

Résumé

Homeostatic scaling of the synapse, such as synaptic down-scaling, has been proposed to offset deleterious effects induced by sustained synaptic strength enhancement. Proper function and subcellular distribution of Src homology 2 domain-containing nonreceptor protein tyrosine phosphatase (SHP2) are required for synaptic plasticity. However, the role of SHP2 in synaptic down-scaling remains largely unknown. Here, using biochemical assays and cell-imaging techniques, we found that synaptic SHP2 levels are temporally regulated during synaptic down-scaling in cultured hippocampal neurons. Furthermore, we observed that a Noonan syndrome-associated mutation of SHP2, resulting in a D61G substitution, prevents synaptic down-scaling. We further show that this effect is due to an inability of the SHP2-D61G variant to properly disassociate from postsynaptic density protein 95, leading to impaired SHP2 dispersion from synaptic sites after synaptic down-scaling. Our findings reveal a molecular mechanism of the Noonan syndrome-associated genetic variant SHP2-D61G that contributes to deficient synaptic down-scaling.

Identifiants

pubmed: 32499374
pii: S0021-9258(17)48941-1
doi: 10.1074/jbc.RA119.010331
pmc: PMC7380183
doi:

Substances chimiques

Disks Large Homolog 4 Protein 0
Dlg4 protein, mouse 0
Protein Tyrosine Phosphatase, Non-Receptor Type 11 EC 3.1.3.48
Ptpn11 protein, mouse EC 3.1.3.48

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

10023-10031

Informations de copyright

© 2020 Lu et al.

Déclaration de conflit d'intérêts

Conflict of interest—The authors declare that they have no conflicts of interest with the contents of this article.

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Auteurs

Wen Lu (W)

Department of Biochemistry and Molecular Biology, Hainan Medical University, Haikou, China.
Key Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, China.

Heng Ai (H)

Department of Physiology, Hangzhou Medical College, Hangzhou, Zhejiang, China.

Fusheng Xue (F)

Zhejiang Key Laboratory of Organ Development and Regeneration, Institute of Life Sciences, Hangzhou Normal University, Hangzhou, Zhejiang, China.

Yifei Luan (Y)

Department of Physiology, Hangzhou Medical College, Hangzhou, Zhejiang, China.

Bin Zhang (B)

Zhejiang Key Laboratory of Organ Development and Regeneration, Institute of Life Sciences, Hangzhou Normal University, Hangzhou, Zhejiang, China zhangbin890124@163.com.

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Classifications MeSH