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JH Kim, J Jensen, T Williams, R Buettner, JA West-Mays; The AP-2 And AP-2ß Genes Participate Together In Controlling Early Lens Development . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3881.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:AP-2α is a critical regulator of lens development (ARVO 1998;2026). An additional AP-2 family member, AP-2ß is co-expressed with AP-2α in the lens placode, and the expression of the AP-2ß gene may compensate for the loss of AP-2α during earlier stages of lens development in the AP-2α null mutant. Thus, it is proposed that the AP-2α and AP-2ß genes participate together in establishing a threshold required for early lens induction. Methods:Lens development in double mutant AP-2α/AP-2ß embryos (E9.5-E15.5) was characterized histologically and immunohistochemically. Results:Double mutation resulted in earlier embryonic lethality (between E12.5 and E15.5) than the single knockout mice. However, to our advantage by E12.5 of mouse embryogenesis significant stages of lens development have already occurred. Double mutant embryos at E9.5 exhibited a broad thickening of the surface ectoderm overlying the optic vesicle, which resembled a lens placode. However, Pax6 expression was substantially reduced as compared to single knockout and wild-type mice. Subsequent stages of lens vesicle formation (E10.5) were severely disrupted, including a dramatic thinning of the placode and formation of a shallow lens pit. Conclusion:These data suggest that redundancy between the two AP-2 genes in early lens formation exists, since lens formation was disrupted at a much earlier stage of development (between E9.5-10.5) in the double mutants as compared to the single AP-2α and AP-2ß mutants. Further studies will determine the specific function of the AP-2 genes in lens placode formation.
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