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Zfp503/Nlz2 Is Required for RPE Differentiation and Optic Fissure Closure
Elangovan Boobalan1, Amy H Thompson1, Ramakrishna P Alur1
1Pediatric, Developmental & Genetic Ophthalmology Section, Ophthalmic Genetics & Visual Function Branch, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Zfp503 gene loss causes uveal coloboma in mice by disrupting retinal pigment epithelium fate and optic fissure closure. This study highlights Zfp503
Area of Science:
- Developmental biology
- Ophthalmology
- Genetics
Background:
- Uveal coloboma is a congenital eye malformation.
- Genetic mutations explain only a minority of cases.
- Zfp503 is implicated in zebrafish eye development.
Purpose of the Study:
- Characterize Zfp503 knockout (KO) mice.
- Investigate Zfp503's role in optic fissure closure.
- Analyze transcriptomic changes in mutant RPE/choroid.
Main Methods:
- Generated Zfp503 KO mice via gene targeting.
- Performed histological and molecular analyses.
- Conducted RNA sequencing of E11.5 RPE/choroid.
Main Results:
- Zfp503 loss causes uveal coloboma in mice.
- Altered expression of key eye development transcription factors observed.
- Reduced melanin synthesis and RPE to neural retina lineage switch occurred.
- RNA sequencing revealed downregulated melanin genes and optic fissure-related genes.
Conclusions:
- Zfp503 is critical for maintaining RPE fate.
- Zfp503 plays a vital role in optic fissure closure.
- Identified Zfp503 as a key gene in eye development.
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