This study investigates the relationship between Pannexin 1 and refractive errors using a custom-made 1310nm OCT system, capable of imaging the whole eye. Prior research reported vision-related issues in Panx1 mutants but lacked insights into underlying mechanisms. Obtained OCT results establish a direct link between Pannexin1 (Pannexin 1a, Pannexin 1b, and Panx1DKO) and eye structure alterations, primarily manifesting as axial length elongation and negative RRE values, indicating myopia. Additionally, whole eye OCT imaging identifies several category of defects in the lens epithelium and aphakia. This research underscores Pannexin1's significance in visual system development and refractive errors, further emphasizing the diagnostic potential of optical coherence tomography in ophthalmology. Leveraging zebrafish as a model organism offers a unique opportunity to investigate genetic and cellular mechanisms influencing eye health, advancing our understanding of genetic factors and paving the way for further research and potential therapeutic interventions in the field of ophthalmology.
Refractive errors, such as myopia and hyperopia, are a major cause of visual impairment worldwide. The genetic basis of refractive errors is becoming increasingly understood, and the zebrafish has emerged as a powerful model organism for studying these disorders. In this study, we present evidence that establishes a connection between the mammalian connexin-36 (Cx36) ortholog gjd2b/Cx35.1, a key component of electrical synapses in zebrafish, as well as connexin-27(Cx27.5), and the occurrence of refractive errors. We investigated the morphological and behavioral changes in adult zebrafish. To assess these changes, we utilized a custom-developed 1310nm optical coherence tomography system for analysis of the entire eye. This analysis revealed development of hyperopic shifts in Cx35.1 knockouts, primarily due to a reduction in eye axial length, while no refractive anomalies were observed in Cx27.5 knockouts.
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