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Neural stem cell gene plays crucial role in eye development

the neural stem cell pool to aberrantly differentiate into neurons during development," Pevny said. "This disrupts the normal maintenance of the stem cell pool in the eye and disrupts the whole developmental process."

A complete loss of SOX2 expression in neural retinal progenitor cells results in the loss of the ability to either differentiate into neurons, or stay in the pluripotent state. In the pluripotent state, the cells are constantly replenished, but each cell retains the ability to differentiate into different cell types. This loss results in a block in eye formation in mice.

The manuscript also describes that one of the genes that SOX2 controls is Notch1, and loss of regulation of this gene is what is partially responsible for abnormal development of the eye. Notch1 is expressed in several other stem cell/progenitor populations. Therefore, SOX2 may play an important role in maintaining these populations as well.

In addition to highlighting a role for SOX2 in normal eye development, Pevny also stressed that this study illustrates the power of mouse genetics. "Right now, we are only in the hypothetical stage of therapeutic application of this work, but we finally have the genetic tools to actually test our hypothesis."

Other authors that contributed to the study are members of the UNC Neuroscience Center and department of genetics: Dr. Olena Taranova, a former UNC graduate student in neurobiology, now a postdoctoral scientist in the UNC Lineberger Comprehensive Cancer Center; Dr. Scott T. Magness, a postdoctoral scientist; B. Matthew Fagan, research technician; Dr.Yongquin Wu, director of the In Situ Hybridization Core Facility at the UNC Neuroscience Center; and Scott R. Hutton and Natalie Surzenko, graduate research assistants in the UNC Neurobiology Curriculum.

This work is supported by grants from the National Institutes of Health and the Christopher Reeves Paralysis Foundation


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Source:University of North Carolina School of Medicine


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