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Pax2 expression and retinal morphogenesis in the normal and Krd mouse
D C Otteson1, E Shelden, J M Jones
1Department of Anatomy and Cell Biology, University of Michigan, Ann Arbor 48105, USA.
Developmental Biology
|March 7, 1998
Summary
Pax2 haploinsufficiency in Krd/+ mice causes abnormal development of the optic fissure and optic disc. This leads to structural defects in the retina and optic disc, impacting vision.
Area of Science:
- Developmental biology
- Genetics
- Ophthalmology
Background:
- The Kidney and retinal defects (Krd) mouse model exhibits kidney and retinal defects due to a deletion including the Pax2 locus.
- Heterozygous Krd/+ mice are haploid for Pax2, displaying a semidominant phenotype with variable renal and ocular anomalies.
- Pax2 haploinsufficiency is hypothesized to underlie the Krd phenotype, mirroring human conditions.
Purpose of the Study:
- To investigate the embryonic origins of ocular defects in Krd/+ mice.
- To analyze Pax2 protein distribution and its role in ocular development during embryogenesis.
Main Methods:
- Immunohistochemistry to detect Pax2 protein distribution.
- Digital three-dimensional reconstructions for detailed structural analysis.
- Quantitative morphometry to measure developmental parameters.
Main Results:
- In normal embryos, Pax2+ cells define the embryonic fissure and optic disc.
- Krd/+ embryos show abnormal morphogenetic movements of Pax2+ cells in the optic cup and stalk.
- Failure of normal embryonic fissure formation and abnormal organization of Pax2+ cells and axons at the optic disc were observed.
Conclusions:
- Abnormal Pax2+ cell movements and initial axon misrouting in Krd/+ embryos cause retinal and optic disc defects.
- These embryonic anomalies explain the ocular phenotypes observed in adult Krd/+ mice.
- The study highlights Pax2's critical role in mammalian eye development.