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Large is required for normal astrocyte migration and retinal vasculature development
Min Zhou1,2, Herui Wang3,4, Hui Ren1,2
1Department of Ophthalmology, Eye and ENT Hospital of Fudan University, Shanghai, 200031 China.
Cell & Bioscience
|April 22, 2017
Summary
A novel LARGE mutation causes persistent fetal vasculature (PFV) and abnormal retinal vasculature in mice. This study reveals LARGE
Area of Science:
- Ophthalmology
- Developmental Biology
- Genetics
Background:
- Persistent fetal vasculature (PFV) is a congenital eye anomaly causing childhood blindness.
- The molecular basis of PFV is not fully understood.
- LARGE mutations are linked to muscle-eye-brain disorders, but its role in eye vasculature is unclear.
Purpose of the Study:
- To investigate the role of LARGE in ocular vasculature development.
- To characterize a novel LARGE mutation causing PFV in mice.
Main Methods:
- Generated a novel LARGE mutation using piggyBac transposon insertion in mice.
- Analyzed retinal vasculature and astrocyte distribution in LARGE mutants.
Main Results:
- A novel LARGE mutation induced PFV and abnormal retinal vasculature.
- Impaired glycosylation of α-dystroglycan (α-DG) led to a broken inner limiting membrane (ILM).
- Retinal astrocytes exhibited irregular distribution and abnormal migration into the vitreous.
Conclusions:
- LARGE is crucial for ILM formation and regulating retinal astrocyte migration.
- The novel LARGE mutant mouse provides a new model for studying PFV and LARGE function in ocular development.
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