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Sabine Fuhrmann

Associate Professor of Neurobiology and Anatomy and of Ophthalmology and Visual Sciences

B.S. University of Oldenburg, Germany

Ph.D. University of Freiburg, Germany

Research

References

sabine.fuhrmann@hsc.utah.edu

Sabine Fuhrmann's PubMed Literature Search

Research

The goal of our research is to understand the cellular and molecular mechanisms that regulate the patterning and differentiation of the vertebrate eye. Questions addressed in our lab include: How is eye development initiated in the anterior neuroepithelium and what factors determine the early steps of eye formation? How is differentiation of ocular tissues controlled? What are the signals involved in these processes and what are their downstream targets? Is there crosstalk between different pathways? How is homeostasis of ocular tissues maintained?

The vertebrate eye is formed through coordinated interactions between neuroepithelium, surface ectoderm, and extraocular mesenchyme. Following eye field formation, the neuroepithelium of the ventral forebrain evaginates, resulting in the formation of bilateral optic vesicles. Factors from surrounding tissues, extracellular factors and intrinsic signals such as transcription factors, control differentiation of the neural retina and retinal pigment epithelium (RPE) starting at the early optic vesicle stage.

One major focus in the lab is to investigate how the RPE develops. In the adult, the RPE is located between the retina and choroid in the posterior eye and consists of a monolayer of cuboidal, pigmented cells. It is vital for growth of the eye; improper develop­ment results in congenital ocular defects such as microphthalmia, anophthalmia or a change of cell fate resulting in loss of the RPE. Moreover, the RPE is absolutely critical for photoreceptor function and homeostasis in the adult eye. Thus, a better understanding of the mechanisms underlying RPE development and homeostasis may provide a basis for therapeutic treatments of ocular diseases such as macular degeneration and will be important for ocular stem cell biology. However, very little is known about the mechanisms that specify and maintain the RPE fate. We use conditional inactivation in mice in combination with tissue culture and biochemical and cell biological approaches to test the function of TGFb/Activin and Wnt signaling in RPE induction and differentiation as well as in RPE homeostasis in the adult eye.

Conditional disruption of ß-catenin in the embryonic mouse RPE leads to a loss of pigmentation (B; arrow) and abnormal thickening of the dorsal RPE (D; arrowhead), an initial sign of defective RPE formation. A,C: control eyes.

References