Document Type
Article
Publication Date
9-2-2025
Original Citation
Tolman N,
Simón M,
Juarez F,
Zhang C,
Hristova Z,
Ouellette T,
Sellarole M,
deVries W,
Montgomery C,
John S.
Absence of Glaucoma in Tg-MYOCY437H Mice of Diverse Genetic Backgrounds. Invest Ophthalmol Vis Sci. 2025;66(12):40.
Keywords
JMG, SS1, Animals, Mice, Eye Proteins, Intraocular Pressure, Cytoskeletal Proteins, Glaucoma, Glycoproteins, Mice, Transgenic, Phenotype, Disease Models, Animal, Mice, Inbred C57BL, Mutation, Genetic Background
JAX Source
Invest Ophthalmol Vis Sci. 2025;66(12):40.
ISSN
1552-5783
PMID
40965407
DOI
https://doi.org/10.1167/iovs.66.12.40
Grant
Supported partially by National Eye Institute grants EY011721, EY032507, EY032062, and EY018606 (S.W.M.J).
Abstract
PURPOSE: Mutations in the myocilin (MYOC) gene cause elevated intraocular pressure and glaucoma. To better understand the factors influencing susceptibility to glaucoma, we studied the MYOC mutation (MYOCY437H).
METHODS: We characterized ocular phenotypes in Tg-MYOCY437H mice on nine different mouse strain backgrounds.
RESULTS: No glaucoma-related phenotypes were observed. We detected neither elevated intraocular pressure (daytime readings) nor optic nerve degeneration differences between wild type (WT) and Tg-MYOCY437H mice. This included an absence of Tg-MYOCY437H-induced phenotypes on a mixed B6SJL background that best reflected the original publications with this strain. We confirmed that this result was not due to an absence of transgene expression in ocular tissues.
CONCLUSIONS: Our data indicate undefined complexity and that the previously reported glaucoma phenotypes are not robust across all institutions and environments.
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.