Glycolytic reliance promotes anabolism in photoreceptors
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Abstract
Sensory neurons capture information from the environment and convert it into signals that can greatly impact the survival of an organism. These systems are thus under heavy selective pressure, including for the most efficient use of energy to support their sensitivity and efficiency 1 . In this regard, the vertebrate photoreceptor cells face a dual challenge. They not only need to preserve their membrane excitability via ion pumps by ATP hydrolysis 2 but also maintain a highly membrane rich organelle, the outer segment, which is the primary site of phototransduction, creating a considerable biosynthetic demand. How photoreceptors manage carbon allocation to balance their catabolic and anabolic demands is poorly understood. One metabolic feature of the retina is its ability to convert the majority of its glucose into lactate 3,4 even in the presence of oxygen. This phenomenon, aerobic glycolysis, is found in cancer and proliferating cells, and is thought to promote biomass buildup to sustain proliferation 5,6 . The purpose of aerobic glycolysis in the retina, its relevance to photoreceptor physiology, and its regulation, are not understood. Here, we show that rod photoreceptors rely on glycolysis for their outer segment (OS) biogenesis. Genetic perturbations targeting allostery or key regulatory nodes in the glycolytic pathway impacted the OS size. Fibroblast growth factor (FGF) signaling was found to regulate glycolysis, with antagonism of this pathway resulting in anabolic deficits. These data demonstrate the cell autonomous role of the glycolytic pathway in OS maintenance and provide evidence that aerobic glycolysis is part of a metabolic program that supports the biosynthetic needs of a normal neuronal cell type.
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The high level of glycolysis in photoreceptors is important as they perform substantial biosynthesis during their diurnal degradation and nocturnal regeneration of outer segments.
“The high level of glycolysis in photoreceptors is important as they perform substantial biosynthesis during their diurnal degradation and nocturnal regeneration of outer segments (Chinchore et al., 2017).”
From Fueling thought: Management of glycolysis and oxidative phosphorylation in neuronal metabolism (2018) · cites this paper as Chinchore et al., 2017
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- Authors
- Chinchore, Y., Begaj, T., Wu, D., Drokhlyansky, E., & Cepko, C. L.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Cepko, Constance L
- Venue
- eLife
- Publisher
- eLife Sciences Publications, Ltd
- Published
- 2017-06-09
- Volume
- 6
- ISSN
- 2050-084X (ISSN-L)
- PMC
- PMC5499945
- OpenAlex
- W2590528398
- Cited by
- 191
- References
- 67
- Citations by year
- 2026: 27 · 2025: 20 · 2024: 25 · 2023: 19 · 2022: 21 · 2021: 23 · 2020: 24 · 2019: 12 · 2018: 15 · 2017: 4 · 2013: 1
- FWCI
- 6.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- eLife (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (R01 EY023291)
- Howard Hughes Medical Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- rod photoreceptors, glycolysis, aerobic glycolysis, phototransduction, anabolism, FGF signaling, allosteric regulation, cellular metabolism, ATP consumption
- MeSH terms
- Aerobiosis, Animals, Organelle Biogenesis, Fibroblast Growth Factors, Glycolysis, Metabolism, Signal Transduction, Retinal Rod Photoreceptor Cells, Mice
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