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Mouse Eye Enucleation for Remote High-throughput Phenotyping

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Published on: November 19, 2011

Heterozygote Wdr36-deficient mice do not develop glaucoma.

Martin Gallenberger¹, Markus Kroeber¹, Loreen März¹

¹Institute of Human Anatomy and Embryology, University of Regensburg, Universitätsstr. 31, D-93053 Regensburg, Germany.

Experimental Eye Research

|September 28, 2014

Summary

This summary is machine-generated.

WDR36 variants are controversial in primary open-angle glaucoma (POAG) pathogenesis. Heterozygous Wdr36-deficient mice show no POAG-related structural or functional eye changes, suggesting WDR36 is not causative in POAG.

Keywords:

Animal model Genetics Primary open-angle glaucoma

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Area of Science:

Genetics
Ophthalmology
Molecular Biology

Background:

WDR36 is a nucleolar protein crucial for 18S rRNA maturation.
Mutations in WDR36 are debated for their role in primary open-angle glaucoma (POAG) pathogenesis.
Homozygous Wdr36 deficiency is embryonic lethal, necessitating study of heterozygous models.

Purpose of the Study:

To investigate the phenotypic consequences of heterozygous Wdr36 deficiency in mice.
To determine if WDR36 sequence variants contribute to the pathogenesis of POAG.
To assess the impact of WDR36 deficiency on ocular structures, optic nerve integrity, and retinal ganglion cell susceptibility.

Main Methods:

Analysis of heterozygous Wdr36-deficient (Wdr36(+/-)) mice.
Assessment of ocular tissue structure, intraocular pressure (IOP), and optic nerve axon counts.
Evaluation of retinal ganglion cell susceptibility to NMDA-induced excitotoxicity.
Study of 18S rRNA maturation in Wdr36(+/-) and transgenic mice.

Main Results:

Wdr36(+/-) mice exhibited reduced Wdr36 mRNA expression but normal ocular tissue structure and optic nerve head morphology.
One-year-old Wdr36(+/-) mice showed no significant differences in IOP or optic nerve axon counts compared to wild-type.
Retinal ganglion cell susceptibility to excitotoxic damage and optic nerve axonal damage after high IOP were similar between Wdr36(+/-) and wild-type mice.
Transgenic expression of mutated WDR36 in Wdr36(+/-) mice did not alter optic nerve axons or excitotoxic damage susceptibility.
18S rRNA maturation was not observably different in Wdr36(+/-) or Del605-607 Wdr36(+/-) mice compared to controls.

Conclusions:

The study's findings in Wdr36(+/-) mice do not support a causative role for WDR36 in POAG pathogenesis.
Reduced WDR36 expression alone does not appear to induce POAG-related phenotypes in mice.
Further research may be needed to elucidate the precise role, if any, of WDR36 variants in human POAG.