In this study, we have created a conditional deletion of AP-2α in the developing mouse lens (Le-AP-2α mutants) to determine the cell-autonomous requirement(s) for AP-2α in lens development. Embryonic and adult Le-AP-2α mutants exhibited defects confined to lens placode derivatives, including a persistent adhesion of the lens to the overlying corneal epithelium (or lens stalk). Expression of known regulators of lens vesicle separation, including Pax6, Pitx3, and Foxe3 was observed in the Le-AP-2α mutant lens demonstrating that these genes do not lie directly downstream of AP-2α. Unlike germ-line mutants, Le-AP-2α mutants did not exhibit defects in the optic cup, further defining the tissue specific role(s) for AP-2α in eye development. Finally, comparative microarray analysis of lenses from the Le-AP-2α mutants vs. wildtype littermates revealed differential expression of 415 mRNAs, including reduced expression of genes important for maintaining the lens epithelial cell phenotype, such as E-cadherin.
- Activating protein-2alpha
- E-cadherin, epidermal growth factor receptor
- Lens development
ASJC Scopus subject areas
- Developmental Biology