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The Neuronal Architecture of Xenopus Retinal Ganglion Cells Is Sculpted by Rho-Family GTPases In Vivo
Open accessAbstract
Dendritogenesis, axonogenesis, pathfinding, and target recognition are all affected in distinct ways when Xenopus retinal ganglion cells (RGCs) are transfected with constitutively active (ca), wild-type (wt), and dominant negative (dn) Rho-family GTPases in vivo. Dendritogenesis required Rac1 and Cdc42 activity. Moreover, ca-Rac1 caused dendrite hyperproliferation. Axonogenesis, in contrast, was inhibited by ca-Rac1. This phenotype was partially rescued by the coexpression of dn cyclin-dependent kinase (Cdk5), a proposed effector of Rac1, suggesting that Rac1 activity must be regulated tightly for normal axonogenesis. Growth cone morphology was particularly sensitive to dn-RhoA and wt-Cdc42 constructs. These also caused targeting errors, such as tectal bypass, suggesting that cytoskeletal rearrangements are involved in target recognition and are transduced by these pathways.
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Albertinazzi, C., Gilardelli, D., Paris, S., Longhi, R., & de Curtis, I. (1998) · The Journal of Cell Biology · doi:10.1083/jcb.142.3.815 · Cited by 93
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Cline, H. T. (2001) · Current Opinion in Neurobiology · doi:10.1016/s0959-4388(00)00182-3 · Cited by 499
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Metadata
- Authors
- Ruchhoeft, M. L., Ohnuma, S.-I., McNeill, L., Holt, C. E., & Harris, W. A.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1999-10-01
- Volume
- 19
- Issue
- 19
- Pages
- 8454-8463
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2104948489
- Cited by
- 197
- References
- 1
- FWCI
- 6.07
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Ruchhoeft, M. L., Ohnuma, S.-I., McNeill, L., Holt, C. E., & Harris, W. A. (1999). The Neuronal Architecture of Xenopus Retinal Ganglion Cells Is Sculpted by Rho-Family GTPases In Vivo. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.19-19-08454.1999
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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