May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Photoreceptor Differentiation Is Inhibited in Activin Loss-of-Function Experiments
Author Affiliations & Notes
  • R. Adler
    Ophthalmology, Johns Hopkins Wilmer Eye Inst, Baltimore, Maryland
  • K. Wahlin
    Ophthalmology, Johns Hopkins Wilmer Eye Inst, Baltimore, Maryland
  • I. Rodriguez
    Retinal Cell and Molecular Biology, National Eye Institute, Bethesda, Maryland
  • E. Moreira
    Retinal Cell and Molecular Biology, National Eye Institute, Bethesda, Maryland
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 4474. doi:
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    • Get Citation

      R. Adler, K. Wahlin, I. Rodriguez, E. Moreira; Photoreceptor Differentiation Is Inhibited in Activin Loss-of-Function Experiments. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4474.

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Abstract

Purpose:: We have previously shown that blocking activin function by over-expression of follistatin in the chick embryo retina causes retinal disorganization and rosette formation. The goal of this study was to investigate whether the structural and molecular differentiation of photoreceptor (PhR) cells can proceed normally under these conditions.

Methods:: Over-expression of follistatin (FS), an activin inhibitor, was accomplished by intraocular injection, on embryonic day (ED) 2.5, of FS-encoding RCAS retrovirus; alkaline phosphatase (AP) was expressed as control. Embryos were sacrificed between ED10-17, and their retinas processed for immunocytochemistry (ICC), or for RNA extraction, cDNA synthesis and quantitative (Q) PCR. Image acquisition was done using a Leica SP2 confocal microscope.

Results:: As we previously reported, disorganization of retinal layers and rosette formation started around ED 10 in FS-treated retinas. When studied by QPCR between ED 11 and ED 16, genes normally expressed early during PhR development, like visinin and IRBP, were unchanged or even increased in FS-treated retinas. By contrast, QPCR of genes like visual pigments and peripherin, which normally begin to be expressed during terminal PhR differentiation (ED14-16), showed marked decreases in FS-treated retinas. In agreement with QPCR data, both in the ONL and within the rosettes of FS-treated retinas the PhRs were visinin (+), but practically always visual pigment (-); they also showed apparent reductions in their outer segments. The synaptic maturation of PhR cells is currently being evaluated.

Conclusions:: Inhibition of activin signaling by FS over-expression causes profound inhibition of terminal differentiation of PhR cells. It is conceivable that these effects could be at least partially mediated by retinal disorganization and rosette formation, but the observation that PhR differentiation is inhibited both in the ONL and within the rosettes appears to argue against this possibility.

Keywords: photoreceptors • retinal development • growth factors/growth factor receptors 
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