Open AccessWnt7b through Frizzled-7 receptor promotes dendrite development by coactivation of CaMKII and JNK
Author(s) -
María Edith Ferrari,
María Eugenia Bernis,
Faye McLeod,
Marina Podpolny,
Romina Paola Coullery,
Inelia M. Casadei,
Patricia C. Salinas,
Silvana Beatriz Rosso
Publication year - 2018
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.216101
Subject(s) - biology , dendrite (mathematics) , wnt signaling pathway , dishevelled , frizzled , microbiology and biotechnology , dendritic spine , neuroscience , signal transduction , hippocampal formation , geometry , mathematics
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 (Dvl) to modulate dendrite arborization by activating a Wnt non-canonical signalling pathway. Here, we identify the seven-transmembrane Frizzled-7 (Fz7) as the receptor for Wnt7b-mediated dendrite growth and complexity. Importantly, Fz7 is developmentally regulated in the intact hippocampus 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 revealed that Wnt7b and Fz7 induce the phosphorylation of CaMKII and JNK, which are required for dendritic development. Here we demonstrate that Wnt7b-Fz7 signals through two Wnt non-canonical pathways to modulate dendritic growth and complexity.