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Chuan-Ming Li, Run-Tao Yan, Shu-Zhen Wang; Atrophy of Müller Glia and Photoreceptor Cells in Chick Retina Misexpressing cNSCL2 . Invest. Ophthalmol. Vis. Sci. 2001;42(13):3103-3109.
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purpose. To investigate whether and how the basic helix-loop-helix (bHLH) gene cNSCL2 is involved in retinal development.
methods. cNSCL2, the chick homologue of human NSCL2, was isolated and sequenced. In situ hybridization
was used to examine its spatial and temporal expression pattern in the
retina. Replication-competent retrovirus RCAS was used to drive cNSCL2 misexpression in the developing chick retina, and
the effect of the misexpression was analyzed.
results. Expression of cNSCL2 in the retina was restricted. Its
mRNA was detected in amacrine and horizontal cells, but not in
photoreceptor, bipolar, or ganglion cells. Retroviral-driven
misexpression of cNSCL2 in the developing chick retina
resulted in missing photoreceptor cells and gross deficits in the outer
nuclear layer (ONL). These deficits were probably not because of
decreased photoreceptor production, in that the ONL appeared normal in
early developmental stages. TUNEL+ cells were detected in
the ONL, indicating that photoreceptor cells underwent apoptosis in
retinas misexpressing cNSCL2. Müller glial cells
were far fewer in the experimental retina than in the control,
indicating that cNSCL2 also caused Müller glia
atrophy. The onset of Müller glia disappearance preceded that of
conclusions. Expression of cNSCL2 in the chick retina was restricted
to amacrine and horizontal cells. Misexpression of cNSCL2 caused severe retinal degeneration, and
photoreceptor cells and Müller glia were particularly
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