PUBLICATION
Slit1b-robo3 signaling and N-cadherin regulate apical process retraction in developing retinal ganglion cells
- Authors
- Wong, G.K., Baudet, M.L., Norden, C., Leung, L., and Harris, W.A.
- ID
- ZDB-PUB-120111-18
- Date
- 2012
- Source
- The Journal of neuroscience : the official journal of the Society for Neuroscience 32(1): 223-2238 (Journal)
- Registered Authors
- Harris, William A., Norden, Caren
- Keywords
- none
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Cadherins/physiology*
- Cell Differentiation/physiology*
- Nerve Tissue Proteins/physiology*
- Receptors, Immunologic/physiology*
- Retina/cytology
- Retina/embryology*
- Retinal Ganglion Cells/cytology
- Retinal Ganglion Cells/metabolism*
- Zebrafish
- Zebrafish Proteins/physiology*
- PubMed
- 22219284 Full text @ J. Neurosci.
Citation
Wong, G.K., Baudet, M.L., Norden, C., Leung, L., and Harris, W.A. (2012) Slit1b-robo3 signaling and N-cadherin regulate apical process retraction in developing retinal ganglion cells. The Journal of neuroscience : the official journal of the Society for Neuroscience. 32(1):223-2238.
Abstract
When neurons exit the cell cycle after their terminal mitosis, they detach from the apical surface of the neuroepithelium. Despite the fact that this detachment is crucial for further neurogenesis and neuronal migration, the underlying mechanisms are still not understood. Here, taking advantage of the genetics and imaging possibilities of the zebrafish retina as a model system, we show by knockdown experiments that the guidance molecule Slit1b and its receptor Robo3 are required for apical retraction of retinal ganglion cells (RGCs). In contrast, N-cadherin seems to be responsible for maintenance of apical attachment, as expression of dominant-negative N-cadherin causes RGCs to lose apical attachments prematurely and rescues retraction in slit1b morphants. These results suggest that Slit-Robo signaling downregulates N-cadherin activity to allow apical retraction in newly generated RGCs
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping