May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
A Comprehensive Negative Regulatory Program Controlled by Brn3b to Ensure Ganglion Cell Specification From Multi-Potential Retinal Precursors
Author Affiliations & Notes
  • F. Qiu
    UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey
    Center for Advanced Biotechnology and Medicine,
  • H. Jiang
    UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey
    Center for Advanced Biotechnology and Medicine,
  • M. Xiang
    UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey
    CABM and Department of Pediatrics,
  • Footnotes
    Commercial Relationships  F. Qiu, None; H. Jiang, None; M. Xiang, None.
  • Footnotes
    Support  EY12020 and EY015777
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 3082. doi:
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    • Get Citation

      F. Qiu, H. Jiang, M. Xiang; A Comprehensive Negative Regulatory Program Controlled by Brn3b to Ensure Ganglion Cell Specification From Multi-Potential Retinal Precursors. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3082.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : The retinal ganglion cells (RGCs) are the sole output neurons in the retina that form the optic nerve and convey light signals detected by photoreceptors to the higher visual system. Their degeneration and damage caused by glaucoma and injury can lead to blindness. During retinogenesis, RGCs are specified from a population of multi-potential precursors capable of generating RGC, amacrine, horizontal and cone cells. How the RGC fate is selected from these multiple neuron fates is unknown at present. We aimed to investigate whether the previously unsuspected POU domain transcription factor Brn3b plays such a critical role.

Methods: : Genetic loss- and gain-of-function analyses were performed in mice at different developmental stages. Meanwhile microarray profiling and other molecular analyses were conducted to investigate the expression network of retinogenic factor genes regulated by Brn3b.

Results: : Loss of Brn3b function in mice leads to mis-specification of early RGC precursors as late-born RGC, amacrine and horizontal cells whereas mis-expressed Brn3b suppresses non-RGC cell fates. Microarray profiling and other molecular analyses reveal that in RGC precursors Brn3b normally represses the expression of a network of retinogenic factor genes involved in fate commitment and differentiation of late-born RGC, amacrine, horizontal, and cone cells.

Conclusions: : Our data suggest that Brn3b specifies the RGC fate from multipotential precursors not only by promoting RGC differentiation but by suppressing non-RGC differentiation programs as a safeguard mechanism.

Keywords: ganglion cells • retinal development • transcription factors 
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