June 2022
Volume 63, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2022
Mitochondria as an Interface for Retinal Development and Disease
Author Affiliations & Notes
  • Mellisa Clemons
    Biological Sciences, University of Idaho, Moscow, Idaho, United States
    Natural Sciences, North Idaho College, Coeur d'Alene, Idaho, United States
  • Dylan Eisenbrandt
    Natural Sciences, North Idaho College, Coeur d'Alene, Idaho, United States
  • Hannah Griffin
    Natural Sciences, North Idaho College, Coeur d'Alene, Idaho, United States
  • Peter Fuerst
    WWAMI Medical Education Program, University of Washington School of Medicine, Moscow, Idaho, United States
  • Footnotes
    Commercial Relationships   Mellisa Clemons None; Dylan Eisenbrandt None; Hannah Griffin None; Peter Fuerst None
  • Footnotes
    Support  NIH Grant #P20GM103408
Investigative Ophthalmology & Visual Science June 2022, Vol.63, 1372 – F0303. doi:
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      Mellisa Clemons, Dylan Eisenbrandt, Hannah Griffin, Peter Fuerst; Mitochondria as an Interface for Retinal Development and Disease. Invest. Ophthalmol. Vis. Sci. 2022;63(7):1372 – F0303.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Mitochondrial dysfunction is linked to retinal degeneration and dysfunction, but basic organization of mitochondria on a cellular and ultrastructural level remains poorly characterized. The mitochondria are critical organelles with roles in energy production, intracellular calcium regulation, and developmental cell death. In this study we complement a basic analysis of mitochondrial organization and ultrastructure with additional comparisons in mutant mouse models.

Methods : Using ImageJ and serial electron micrographs of mouse retina, we performed ultrafine 3D reconstructions of mitochondria in rods and rod bipolar cells (RBCs). We characterized the volume distribution and morphological complexity of individual mitochondria within wild type (WT) retinas. We used One-way ANOVAs with a Tukey Kramer post hoc to compare WT mitochondria with two additional genetic models that both regulate developmental cell death; Bcl2 associated x-protein (Bax-/-) and Down Syndrome Cell Adhesion Molecule – Like 1 (Dscaml1-/-) mutant mice.

Results : Data show that WT and Bax-/- individual mitochondria have larger volumes than Dscaml1-/- mitochondria (p=0.00014) and (p<10-6). Bax-/- mitochondria show increased morphological complexity when compared to Dscaml1-/- mitochondria (p<10-7), with WT mitochondria being more complex than both Bax-/- and Dscaml1-/- mitochondria (p<10-7) and (p<10-6).

Conclusions : Our results provide a characterization of normal mitochondria in the RBCs of WT retinas. This information is essential in further understanding of mitochondrial function in developing and degenerating models. The comparison between WT and Bax-/- show that loss of Bax contributes to the morphological complexity of mitochondria. Initial comparison of Dscaml1-/-, a gene implicated in retinal developmental and degenerative diseases, shows that mitochondrial morphology and volume relies on Dscaml1 expression. Additional studies focused on proteins that interact with Dscaml1 will need to be completed to determine the possible pathways responsible for mitochondrial differences and how these contribute to disease pathology.

This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.

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