June 2020
Volume 61, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2020
Development of Nystagmus in MyoD Knockout Mice
Author Affiliations & Notes
  • Laura Johnson
    Ophthalmology and Visual Neurosciences, University of Minnesota-Twin Cities, Minneapolis, Minnesota, United States
    Molecular, Cellular, Developmental Biology & Genetics Graduate Program, University of Minnesota-Twin Cities, Minnesota, United States
  • Rachel Kueppers
    Ophthalmology and Visual Neurosciences, University of Minnesota-Twin Cities, Minneapolis, Minnesota, United States
  • Linda K McLoon
    Ophthalmology and Visual Neurosciences, University of Minnesota-Twin Cities, Minneapolis, Minnesota, United States
    Neuroscience, University of Minnesota-Twin Cities, Minnesota, United States
  • Footnotes
    Commercial Relationships   Laura Johnson, None; Rachel Kueppers, None; Linda McLoon, None
  • Footnotes
    Support  RO1 EY15313, T32 AR07612
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 5095. doi:
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      Laura Johnson, Rachel Kueppers, Linda K McLoon; Development of Nystagmus in MyoD Knockout Mice. Invest. Ophthalmol. Vis. Sci. 2020;61(7):5095.

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

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Abstract

Purpose : Extraocular muscles (EOM) maintain a large population of activated satellite cells that provide for continuous remodeling throughout life. While limb skeletal muscles have some myonuclear turnover, it is much more limited than seen in the EOM and other craniofacial muscles. MyoD is a myogenic regulatory factor that activates genes required for muscle differentiation. Its expression results in exit from the cell cycle and stable terminal differentiation. In muscles derived from the paraxial head mesoderm MyoD is downstream of expression of Pax7 and Pitx2, both markers of myogenic precursor cells in EOM. We hypothesized that knocking out MyoD would prevent or slow the progression toward integration into existing muscle fibers, reducing the ability of EOM to remodel continuously.

Methods : We used a MyoD knockout mouse to determine the effects of MyoD on EOM and eye movements. Eye tracking using optokinetic nystagmus of MyoD knockouts and their wild type (WT) litter mate controls was performed on an ISCAN device and analyzed using R. Optokinetic nystagmus responses were recorded for each animal. Animals were tested with no stimuli in light and dark conditions, and with rotating bars at a spatial frequency of 0.12cpd and high contrast (100) between light and dark bars.

Results : Of the WT mice tested, before one year of age the optokinetic nystagmus reflex was normal. In the older WT mice, pendular nystagmus and jerk nystagmus were present. In the oldest WT mice, no eye movements were generated. Of the MyoD KO mice tested, only one had a somewhat normal optokinetic nystagmus reflex. Of the others, 5 had pendular nystagmus, 3 had no detectable eye movements, 3 had bouts of jerk and pseudo-pendular jerk nystagmus. In some of the mice, these abnormal movements were followed by bouts of over 10 seconds duration with no eye movements.

Conclusions : In the absence of MyoD expression over time, normal control of the optokinetic nystagmus reflex was significantly impaired. Lack of MyoD led to an increase in abnormal nystagmic eye movements in the knockout mice tested compared to the wild-type mice. We hypothesize that it is likely due to reduced ability of the myofiber to remodel over time. We are currently testing this hypothesis.

This is a 2020 ARVO Annual Meeting abstract.

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