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P. G. Fuerst, A. Koizumi, R. H. Masland, R. W. Burgess; Neurite Arborization and Mosiac Formation in the Mouse Retina Requires the Down Syndrome Cell Adhesion Molecule. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3842.
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© ARVO (1962-2015); The Authors (2016-present)
The molecular cues that direct these processes in the vertebrate retina are not known.
We have identified a mutant mouse model in which organization of the retina is disrupted.
Some types of retinal amacrine cells from mice with a spontaneous mutation in Dscam, a gene encoding an Ig-superfamily member adhesion molecule, have defects in the arborization of processes and the spacing of cell bodies. In the mutant retina, cells that would normally express Dscam have hyperfasciculated processes, preventing them from creating an orderly arbor. The cell bodies of these neurons are randomly distributed or pulled into clumps rather than being spaced in regular mosaics. Retinal ganglion cells also have defects in spacing and dendritic arborization. Ganglion cell axonal pathfinding is normal, although axonal remodeling is observed after eye opening.
Our results indicate that mouse DSCAM mediates isoneuronal selfavoidance for arborization, and heteroneuronal self-avoidance within specific cell types to prevent fasciculation and to preserve mosaic spacing. These functions are highly analogous to those of Drosophila Dscam and Dscam2, and are necessary for establishing orderly retinal circuitry.
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