Facilitative glucose transporter Glut1 is actively excluded from rod outer segments.
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Photoreceptors are among the most metabolically active cells in the body, relying on both oxidative phosphorylation and glycolysis to satisfy their high energy needs. Local glycolysis is thought to be particularly crucial in supporting the function of the photoreceptor's light-sensitive outer segment compartment, which is devoid of mitochondria. Accordingly, it has been commonly accepted that the facilitative glucose transporter Glut1 responsible for glucose entry into photoreceptors is localized in part to the outer segment plasma membrane. However, we now demonstrate that Glut1 is entirely absent from the rod outer segment and is actively excluded from this compartment by targeting information present in its cytosolic C-terminal tail. Our data indicate that glucose metabolized in the outer segment must first enter through other parts of the photoreceptor cell. Consequently, the entire energy supply of the outer segment is dependent on diffusion of energy-rich substrates through the thin connecting cilium that links this compartment to the rest of the cell.
Animals, Genetically Modified
Glucose Transporter Type 1
Mice, Inbred Strains
Photoreceptor Connecting Cilium
Protein Sorting Signals
Retinal Photoreceptor Cell Inner Segment
Rod Cell Outer Segment
Published Version (Please cite this version)10.1242/jcs.072389
Publication InfoGospe, Sidney M; Baker, Sheila A; & Arshavsky, Vadim Y (2010). Facilitative glucose transporter Glut1 is actively excluded from rod outer segments. J Cell Sci, 123(Pt 21). pp. 3639-3644. 10.1242/jcs.072389. Retrieved from https://hdl.handle.net/10161/4190.
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Helena Rubinstein Foundation Distinguished Professor of Ophthalmology
Research conducted in our laboratory is dedicated to understanding how vision is performed on the molecular level. Our most mature direction addresses the function of rod and cone photoreceptors, which are sensory neurons responsible for the detection and primary processing of information entering the eye in the form of photons. Photoreceptors respond to capturing photons by generating electrical signals transmitted to the secondary neurons in the retina and, ultimately, to the brain. Our wor
Assistant Professor of Ophthalmology
Dr. Gospe joined Duke Ophthalmology on August 1, 2017 following his neuro-ophthalmology fellowship training at Duke. His research interests center on developing novel genetic mouse models of severe mitochondrial dysfunction in retinal ganglion cells (RGCs) and other retinal neurons in order to recapitulate the RGC degeneration seen in human optic neuropathies and the poorly understood pigmentary retinopathy that may accompany these diseases. Mitochondria are the powerhouse o
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