Overexpression of a neural-specific rho family GTPase, cRac1B, selectively induces enhanced neuritogenesis and neurite branching in primary neurons
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Rho family GTPases have been implicated in cytoskeletal reorganization during neuritogenesis. We have recently identified a new gene of this family, cRac1B, specifically expressed in the chicken developing nervous system. This GTPase was overexpressed in primary neurons to study the role of cRac1B in the development of the neuronal phenotype. Overexpression of cRac1B induced an increment in the number of neurites per neuron, and dramatically increased neurite branching, whereas overexpression of the highly related and ubiquitous cRac1A GTPase did not evidently affect neuronal morphology. Furthermore, expression of an inactive form of cRac1B strikingly inhibited neurite formation. The specificity of cRac1B action observed in neurons was not observed in fibroblasts, where both GTPases produced similar effects on cell morphology and actin organization, indicating the existence of a cell type-dependent specificity of cRac1B function. Molecular dissection of cRac1B function by analysis of the effects of chimeric cRac1A/cRac1B proteins showed that the COOH-terminal portion of cRac1B is essential to induce increased neuritogenesis and neurite branching. Considering the distinctive regulation of cRac1B expression during neural development, our data strongly support an important role of cRac1B during neuritogenesis, and they uncover new mechanisms underlying the functional specificity of distinct Rho family GTPases.
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RAC3 encodes a Rho family GTPase that enhances neuritogenesis and neurite branching when overexpressed.
“RAC3 (MIM 602050), another example of a gene affected by duplication, encodes a Rho family GTPase that enhances neuritogenesis and neurite branching when overexpressed.64”
From Convergence of genes and cellular pathways dysregulated in autism spectrum disorders (2014) · cites this paper as [64]
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- Authors
- Albertinazzi, C., Gilardelli, D., Paris, S., Longhi, R., & de Curtis, I.
- Affiliations
- IRCCS Ospedale San Raffaele (IT)
- *Cell Adhesion Unit, Department of Biological and Technological Research, San Raffaele Scientific Institute, 20132 Milano, Italy; and ‡Institute of Hormone Chemistry, National Research Council, 20133 Milano, Italy
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 1998-08-10
- Volume
- 142
- Issue
- 3
- Pages
- 815-825
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2148164
- OpenAlex
- W2145197042
- Cited by
- 93
- References
- 42
- Citations by year
- 2022: 3 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 2 · 2016: 2 · 2015: 4 · 2014: 5 · 2013: 1 · 2012: 5
- FWCI
- 2.44
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- Rho GTPases, neurite outgrowth, neurite branching, primary neurons, actin cytoskeleton remodeling, cell type-specific signaling, COOH-terminal domain, neural development
- MeSH terms
- Actins, Amino Acid Sequence, Animals, Binding Sites, Cells, Cultured, Chick Embryo, Cytoskeleton, Neurons, Neuropeptides, Phenotype, Retina, Neurites, Sequence Homology, Amino Acid, GTP-Binding Proteins, GTP Phosphohydrolases, rac GTP-Binding Proteins, rac1 GTP-Binding Protein
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