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Molecular & Cellular Proteomics 8:1206-1218, 2009.
© 2009 by The American Society for Biochemistry and Molecular Biology, Inc.

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Research

The Thioredoxin-like Protein Rod-derived Cone Viability Factor (RdCVFL) Interacts with TAU and Inhibits Its Phosphorylation in the Retina^*,

Ram Fridlich, Francois Delalande, Céline Jaillard, Jun Lu^¶, Laetitia Poidevin^||, Thérèse Cronin, Ludivine Perrocheau, Géraldine Millet-Puel, Marie-Laure Niepon, Olivier Poch^,||, Arne Holmgren^¶, Alain Van Dorsselaer, Jose-Alain Sahel and Thierry Léveillard^,**

From the Institut de la Vision, INSERM UMR592, 17 rue Moreau, 75012 Paris, France,
Laboratoire de Spectrométrie de Masse Bio-Organique, Institut Pluridisciplinaire Hubert Curien-Département Sciences Analytiques et Interactions Ioniques et Biomoléculaires, Université Louis Pasteur, CNRS, UMR7178, 25 rue Becquerel, 67087 Strasbourg, France,
¶Department of Medical Biochemistry and Biophysics, Medical Nobel Institute for Biochemistry, Karolinska Institute, SE-17177 Stockholm, Sweden, and
||Laboratoire de Bioinformatique et Génomique Intégratives, Institut de Génétique et de Biologie Moléculaire et Cellulaire, 67404 Illkirch, France

Rod-derived cone viability factor (RdCVF) is produced by the Nxnl1 gene that codes for a second polypeptide, RdCVFL, by alternative splicing. Although the role of RdCVF in promoting cone survival has been described, the implication of RdCVFL, a putative thioredoxin enzyme, in the protection of photoreceptors is presently unknown. Using a proteomics approach we identified 90 proteins interacting with RdCVFL including the microtubule-binding protein TAU. We demonstrate that the level of phosphorylation of TAU is increased in the retina of the Nxnl1^–/– mice as it is hyperphosphorylated in the brain of patients suffering from Alzheimer disease, presumably in some cases through oxidative stress. Using a cell-based assay, we show that RdCVFL inhibits TAU phosphorylation. In vitro, RdCVFL protects TAU from oxidative damage. Photooxidative stress is implicated in retinal degeneration, particularly in retinitis pigmentosa, where it is considered to be a contributor to secondary cone death. The functional interaction between RdCVFL and TAU described here is the first characterization of the RdCVFL signaling pathway involved in neuronal cell death mediated by oxidative stress.

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