Home > Publications Database > Wnt7b signalling through Frizzled-7 receptor promotes dendrite development by coactivating CaMKII and JNK. > print

001     140176
005     20240321220747.0
024 7 _ |a 10.1242/jcs.216101
|2 doi
024 7 _ |a pmid:29898920
|2 pmid
024 7 _ |a 0021-9533
|2 ISSN
024 7 _ |a 0370-2952
|2 ISSN
024 7 _ |a 1477-9137
|2 ISSN
024 7 _ |a altmetric:63726834
|2 altmetric
037 _ _ |a DZNE-2020-06498
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Ferrari, María E
|b 0
245 _ _ |a Wnt7b signalling through Frizzled-7 receptor promotes dendrite development by coactivating CaMKII and JNK.
260 _ _ |a Cambridge
|c 2018
|b Company of Biologists Limited
264 _ 1 |3 online
|2 Crossref
|b The Company of Biologists
|c 2018-06-13
264 _ 1 |3 print
|2 Crossref
|b The Company of Biologists
|c 2018-07-01
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1587722037_21495
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a The formation of complex dendritic arbors is crucial for the assembly of functional networks as abnormal dendrite formation underlies several neurodevelopmental and psychiatric disorders. Many extracellular factors have been postulated as regulators of dendritic growth. Wnt proteins play a critical role in neuronal development and circuit formation. We previously demonstrated that Wnt7b acts through the scaffold protein dishevelled 1 (Dvl1) to modulate dendrite arborisation by activating a non-canonical Wnt signalling pathway. Here, we identify the seven-transmembrane frizzled-7 (Fz7, also known as FZD7) as the receptor for Wnt7b-mediated dendrite growth and complexity. Importantly, Fz7 is developmentally regulated in the intact hippocampus, and is localised along neurites and at dendritic growth cones, suggesting a role in dendrite formation and maturation. Fz7 loss-of-function studies demonstrated that Wnt7b requires Fz7 to promote dendritic arborisation. Moreover, in vivo Fz7 loss of function results in dendritic defects in the intact mouse hippocampus. Furthermore, our findings reveal that Wnt7b and Fz7 induce the phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and JNK proteins, which are required for dendritic development. Here, we demonstrate that Wnt7b-Fz7 signals through two non-canonical Wnt pathways to modulate dendritic growth and complexity.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
|0 G:(DE-HGF)POF3-342
|c POF3-342
|f POF III
|x 0
536 _ _ |a 341 - Molecular Signaling (POF3-341)
|0 G:(DE-HGF)POF3-341
|c POF3-341
|f POF III
|x 1
542 _ _ |i 2019-01-01
|2 Crossref
|u http://www.biologists.com/user-licence-1-1/
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Dishevelled Proteins
|2 NLM Chemicals
650 _ 7 |a Dvl1 protein, mouse
|2 NLM Chemicals
650 _ 7 |a Fzd7 protein, mouse
|2 NLM Chemicals
650 _ 7 |a Proto-Oncogene Proteins
|2 NLM Chemicals
650 _ 7 |a Receptors, G-Protein-Coupled
|2 NLM Chemicals
650 _ 7 |a Wnt Proteins
|2 NLM Chemicals
650 _ 7 |a Wnt7b protein, mouse
|2 NLM Chemicals
650 _ 7 |a Calcium-Calmodulin-Dependent Protein Kinase Type 2
|0 EC 2.7.11.17
|2 NLM Chemicals
650 _ 7 |a MAP Kinase Kinase 4
|0 EC 2.7.12.2
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Calcium-Calmodulin-Dependent Protein Kinase Type 2: genetics
|2 MeSH
650 _ 2 |a Calcium-Calmodulin-Dependent Protein Kinase Type 2: metabolism
|2 MeSH
650 _ 2 |a Dendrites: enzymology
|2 MeSH
650 _ 2 |a Dendrites: genetics
|2 MeSH
650 _ 2 |a Dendrites: metabolism
|2 MeSH
650 _ 2 |a Dishevelled Proteins: genetics
|2 MeSH
650 _ 2 |a Dishevelled Proteins: metabolism
|2 MeSH
650 _ 2 |a Hippocampus: growth & development
|2 MeSH
650 _ 2 |a Hippocampus: metabolism
|2 MeSH
650 _ 2 |a MAP Kinase Kinase 4: genetics
|2 MeSH
650 _ 2 |a MAP Kinase Kinase 4: metabolism
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Neurites: metabolism
|2 MeSH
650 _ 2 |a Protein Binding
|2 MeSH
650 _ 2 |a Proto-Oncogene Proteins: genetics
|2 MeSH
650 _ 2 |a Proto-Oncogene Proteins: metabolism
|2 MeSH
650 _ 2 |a Rats
|2 MeSH
650 _ 2 |a Rats, Wistar
|2 MeSH
650 _ 2 |a Receptors, G-Protein-Coupled: genetics
|2 MeSH
650 _ 2 |a Receptors, G-Protein-Coupled: metabolism
|2 MeSH
650 _ 2 |a Wnt Proteins: genetics
|2 MeSH
650 _ 2 |a Wnt Proteins: metabolism
|2 MeSH
650 _ 2 |a Wnt Signaling Pathway
|2 MeSH
700 1 _ |a Bernis, María E
|0 P:(DE-2719)2810557
|b 1
|u dzne
700 1 _ |a McLeod, Faye
|b 2
700 1 _ |a Podpolny, Marina
|b 3
700 1 _ |a Coullery, Romina P
|b 4
700 1 _ |a Casadei, Inelia M
|b 5
700 1 _ |a Salinas, Patricia C
|b 6
700 1 _ |a Rosso, Silvana B
|0 P:(DE-HGF)0
|b 7
|e Corresponding author
773 1 8 |a 10.1242/jcs.216101
|b : The Company of Biologists, 2018-06-13
|n 13
|p jcs216101
|3 journal-article
|2 Crossref
|t Journal of Cell Science
|v 131
|y 2018
|x 0021-9533
773 _ _ |a 10.1242/jcs.216101
|g Vol. 131, no. 13, p. jcs216101 -
|0 PERI:(DE-600)1483099-1
|n 13
|q 131:13|p jcs216101
|t Journal of cell science
|v 131
|y 2018
|x 0021-9533
909 C O |o oai:pub.dzne.de:140176
|p VDB
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 1
|6 P:(DE-2719)2810557
913 1 _ |a DE-HGF
|b Forschungsbereich Gesundheit
|l Erkrankungen des Nervensystems
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|v Disease Mechanisms and Model Systems
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913 1 _ |a DE-HGF
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|v Molecular Signaling
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914 1 _ |y 2018
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Marc 21