Wimberg, Hanna and Janssen-Bienhold, Ulrike and Koch, Karl-Wilhelm (2018) Control of the nucleotide cycle in photoreceptor cell extracts by retinal degeneration protein 3. Frontiers in molecular neuroscience, 11. p. 52. ISSN 1662-5099

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Official URL: http://dx.doi.org/10.3389/fnmol.2018.00052

Abstract

Retinal degeneration protein 3 (RD3) is crucial for photoreceptor cell survival and linked to Leber Congenital Amaurosis type 12 (LCA12), a hereditary retinal disease in humans. RD3 inhibits photoreceptor guanylate cyclases GC-E and GC-F and is involved in transport of GCs from the inner to the outer segments. Otherwise, its role in photoreceptor physiology is poorly understood. Here, we describe a new function of RD3. Purified RD3 evoked an increase in guanylate kinase activity, an enzyme that is involved in the nucleotide cycle in photoreceptors. We demonstrate a direct interaction between guanylate kinase and RD3 using back-scattering interferometry and show by immunohistochemistry of mouse retina sections that RD3 and guanylate kinase co-localize in photoreceptor inner segments and to a lesser extent in the outer plexiform layer. Our findings point toward a more complex function of RD3 in photoreceptors. The RD3 – guanylate kinase interaction may also play a role in other cellular systems, while the GC – RD3 interaction is exclusive to photoreceptors.

Item Type: Article
Additional Information: Publiziert mit Hilfe des DFG-geförderten Open Access-Publikationsfonds der Carl von Ossietzky Universität Oldenburg.
Uncontrolled Keywords: RD3 protein, guanylate kinase, retinal dystrophy, cyclic nucleotide, phototransduction
Subjects: Science and mathematics > Chemistry
Science and mathematics > Life sciences, biology
Technology, medicine, applied sciences > Medicine and health
Divisions: Faculty of Medicine and Health Sciences > Department of Neuro Sciences
Date Deposited: 10 Sep 2019 09:12
Last Modified: 12 Sep 2019 11:39
URI: https://oops.uni-oldenburg.de/id/eprint/4125
URN: urn:nbn:de:gbv:715-oops-42068
DOI: doi:10.3389/fnmol.2018.00052
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