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Rod-derived Cone Viability Factor

ABSTRACT: Rod-derived Cone Viability Factor stimulates aerobic glycolysis through BSG1/GLUT1

INSTRUMENT(S): Bruker Daltonics HCT Series, maXis

ORGANISM(S): Gallus Gallus (chicken)

TISSUE(S): Embryo

SUBMITTER: Francois Delalande

LAB HEAD: Delalande Francois

PROVIDER: PXD001384 | Pride | 2016-06-15

REPOSITORIES: Pride

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Rod-derived cone viability factor promotes cone survival by stimulating aerobic glycolysis.

Aït-Ali Najate N Fridlich Ram R Millet-Puel Géraldine G Clérin Emmanuelle E Delalande François F Jaillard Céline C Blond Frédéric F Perrocheau Ludivine L Reichman Sacha S Byrne Leah C LC Olivier-Bandini Anne A Bellalou Jacques J Moyse Emmanuel E Bouillaud Frédéric F Nicol Xavier X Dalkara Deniz D van Dorsselaer Alain A Sahel José-Alain JA Léveillard Thierry T

Cell 20150501 4

Rod-derived cone viability factor (RdCVF) is an inactive thioredoxin secreted by rod photoreceptors that protects cones from degeneration. Because the secondary loss of cones in retinitis pigmentosa (RP) leads to blindness, the administration of RdCVF is a promising therapy for this untreatable neurodegenerative disease. Here, we investigated the mechanism underlying the protective role of RdCVF in RP. We show that RdCVF acts through binding to Basigin-1 (BSG1), a transmembrane protein expressed ...[more]

PMID: 25957687

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Rod-derived Cone Viability Factor 2

Project description:Rod-derived Cone Viability Factor (RdCVF) is a truncated thioredoxin secreted by rod photoreceptors that protects cones. Because the secondary loss of cones in retinitis pigmentosa (RP) is the major visual handicap of this untreatable neurodegenerative disease, the administration of RdCVF is thought to be a promising therapy for RP. We show that RdCVF is acting by binding to Basigin-1 (BSG1) at the surface of cones. BSG1 is an alternative splice product of the BSG gene, a transmembrane protein with an extra immunoglobin domain expressed specifically in the retina. BSG1 binds to the glucose transporter GLUT1. RdCVF increases glucose entry into cones. We found that the increase in glucose is used by cones to induce cell survival by stimulating aerobic glycolysis. A disease associated missense mutation of RdCVF results in its inability to bind to BSG1, to stimulate glucose uptake and to prevent secondary cone death of a model of RP.

2016-06-15 | PXD001715 | Pride

Susceptibility to photo-oxidative damage of mice lacking the Rod derived Cone Viability Factor gene Nxnl1

Project description:Rod-derived Cone Viability Factor is a trophic factor of the thioredoxins family that promotes the survival of cone photoreceptors. It is encoded by the nucleoredoxin-like gene 1 Nxnl1 which also encodes by alternative splicing for RdCVFL, for a thioredoxin enzyme that interacts with the protein TAU. The role of thioredoxins in the defense mechanism against oxidation led us to examine the retinal phenotype of the Nxnl1-/- mouse after photo-oxidative stress. In total 16 samples were analyzed, they represent two different genotypes (wt/wt, ko/ko) both on pure BALB/c background and two doses of light that were tested in triplicate each.

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Susceptibility to photo-oxidative damage of mice lacking the Rod derived Cone Viability Factor gene Nxnl1

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Identification of rod- and cone-specific expression signatures to identify candidate genes for retinal disease

Project description:Exon array analysis was performed using retinae from three transgenic mouse models, coneless (cl), rodless (rd/rd) and rodless/coneless (rd/rd cl) compared to wildtype (non-rd) allowing gene expression in the rod and cone photoreceptors to be examined.

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Project description:Cone photoreceptors are the primary initiator of visual transduction in the human retina. Dysfunction or death of rod photoreceptors precedes cone loss in many retinal and macular degenerative diseases, suggesting a rod-dependent trophic support for cone survival. Rod differentiation and homeostasis are dependent on the basic motif leucine zipper transcription factor NRL. The loss of Nrl in mice (Nrl-/-) results in a retina with predominantly S-opsin containing cones that exhibit molecular and functional characteristics of WT cones. Here we report that Nrl-/- retina undergoes a rapid but transient period of degeneration in early adulthood, with cone apoptosis, retinal detachment, alterations in retinal vessel structure, and activation and translocation of retinal microglia. However, cone degeneration stabilizes by four months of age, resulting in a thinned but intact outer nuclear layer with residual cones expressing S- and M-opsins and a preserved photopic ERG. At this stage, microglia translocate back to the inner retina and reacquire a quiescent morphology. Gene profiling analysis during the period of transient degeneration reveals misregulation of stress response and inflammation genes, implying their involvement in cone death. The Nrl-/- retina illustrates the long-term viability of cones in the absence of rods and may serve as a model for elucidating mechanisms of cone homeostasis and degeneration that would be relevant to understanding diseases of the cone-dominant human macula. Targets were generated from a pair of retinas (one Nrl-/- mouse) per biological replicate. Four biological replicates were generated for each of the five aging timepoints (1, 2, 4, 6, and 10 months post natal).

2011-11-15 | E-GEOD-33674 | biostudies-arrayexpress

Transcriptome dynamics of developing photoreceptors in 3-D retina cultures recapitulates temporal sequence of human cone and rod differentiation revealing cell surface markers and gene networks

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Increased H3K27 trimethylation contributes to cone survival in a mouse model of cone dystrophy

Project description:Inherited retinal diseases (IRDs) are a heterogeneous group of blinding disorders, which result in dysfunction or death of the light-sensing cone and rod photoreceptors. Despite individual IRDs being rare, collectively they affect up to 1:2000 people worldwide, causing a significant socioeconomic burden, especially when cone-mediated central vision is affected. This study uses the Pde6ccpfl1 mouse model of achromatopsia, a cone-specific vision loss IRD, to investigate the potential gene-independent therapeutic benefits of a histone demethylase inhibitor GSK-J4 on cone cell survival. We investigated the effects of GSK-J4 treatment on cone cell survival in vivo and ex vivo and changes in cone-specific gene expression via single-cell RNA sequencing. A single intravitreal GSK-J4 injection led to transcriptional changes in pathways involved in mitochondrial dysfunction, endoplasmic reticulum stress, among other key epigenetic pathways, highlighting the complex interplay between methylation and acetylation in healthy and diseased cones. Furthermore, continuous administration of GSK-J4 in retinal explants increased cone survival. Our results suggest that IRD-affected cones respond positively to epigenetic modulation of histones, indicating the potential of this approach in the development of a broad class of novel therapies to slow cone degeneration.

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