Senior Scholars Program

UMMS Affiliation

School of Medicine; Senior Scholars Program

Faculty Advisor

Connie Cepko

Publication Date

2017-06-09

Document Type

Article

Disciplines

Biochemical Phenomena, Metabolism, and Nutrition | Cell Biology | Cellular and Molecular Physiology | Medical Education | Neuroscience and Neurobiology

Abstract

Vertebrate photoreceptors are among the most metabolically active cells, exhibiting a high rate of ATP consumption. This is coupled with a high anabolic demand, necessitated by the diurnal turnover of a specialized membrane-rich organelle, the outer segment, which is the primary site of phototransduction. How photoreceptors balance their catabolic and anabolic demands is poorly understood. Here, we show that rod photoreceptors in mice rely on glycolysis for their outer segment biogenesis. Genetic perturbations targeting allostery or key regulatory nodes in the glycolytic pathway impacted the size of the outer segments. Fibroblast growth factor 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 outer segment maintenance and provide evidence that aerobic glycolysis is part of a metabolic program that supports the biosynthetic needs of a normal neuronal cell type.

Keywords

Warburg effect, allostery, cell biology, mouse, neuroscience, outer segments, retinal metabolism

Rights and Permissions

Copyright Chinchore et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

DOI of Published Version

10.7554/eLife.25946

Source

Elife. 2017 Jun 9;6. doi: 10.7554/eLife.25946. Link to article on publisher's site

Journal/Book/Conference Title

eLife

Comments

Tedi Begaj participated in this study as a medical student as part of the Senior Scholars research program at the University of Massachusetts Medical School.

Related Resources

Link to Article in PubMed

PubMed ID

28598329

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

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