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@ARTICLE{Ferrari:140176,
      author       = {Ferrari, María E and Bernis, María E and McLeod, Faye and
                      Podpolny, Marina and Coullery, Romina P and Casadei, Inelia
                      M and Salinas, Patricia C and Rosso, Silvana B},
      title        = {{W}nt7b signalling through {F}rizzled-7 receptor promotes
                      dendrite development by coactivating {C}a{MKII} and {JNK}.},
      journal      = {Journal of cell science},
      volume       = {131},
      number       = {13},
      issn         = {0021-9533},
      address      = {Cambridge},
      publisher    = {Company of Biologists Limited},
      reportid     = {DZNE-2020-06498},
      pages        = {jcs216101},
      year         = {2018},
      abstract     = {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.},
      keywords     = {Animals / Calcium-Calmodulin-Dependent Protein Kinase Type
                      2: genetics / Calcium-Calmodulin-Dependent Protein Kinase
                      Type 2: metabolism / Dendrites: enzymology / Dendrites:
                      genetics / Dendrites: metabolism / Dishevelled Proteins:
                      genetics / Dishevelled Proteins: metabolism / Hippocampus:
                      growth $\&$ development / Hippocampus: metabolism / MAP
                      Kinase Kinase 4: genetics / MAP Kinase Kinase 4: metabolism
                      / Mice / Mice, Inbred C57BL / Neurites: metabolism / Protein
                      Binding / Proto-Oncogene Proteins: genetics / Proto-Oncogene
                      Proteins: metabolism / Rats / Rats, Wistar / Receptors,
                      G-Protein-Coupled: genetics / Receptors, G-Protein-Coupled:
                      metabolism / Wnt Proteins: genetics / Wnt Proteins:
                      metabolism / Wnt Signaling Pathway / Dishevelled Proteins
                      (NLM Chemicals) / Dvl1 protein, mouse (NLM Chemicals) / Fzd7
                      protein, mouse (NLM Chemicals) / Proto-Oncogene Proteins
                      (NLM Chemicals) / Receptors, G-Protein-Coupled (NLM
                      Chemicals) / Wnt Proteins (NLM Chemicals) / Wnt7b protein,
                      mouse (NLM Chemicals) / Calcium-Calmodulin-Dependent Protein
                      Kinase Type 2 (NLM Chemicals) / MAP Kinase Kinase 4 (NLM
                      Chemicals)},
      cin          = {AG Tamgüney 2},
      ddc          = {570},
      cid          = {I:(DE-2719)1013022},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 341
                      - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29898920},
      doi          = {10.1242/jcs.216101},
      url          = {https://pub.dzne.de/record/140176},
}