April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Ap-2α Plays Role In Lens Epithelial Cell Maintenance Subsequent To Lens Vesicle Separation
Author Affiliations & Notes
  • Christine L. Kerr
    Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
  • Mizna Zaveri
    Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
  • Michael L. Robinson
    Zoology, Miami University, Oxford, Ohio
  • Judith A. West-Mays
    Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
  • Footnotes
    Commercial Relationships  Christine L. Kerr, None; Mizna Zaveri, None; Michael L. Robinson, None; Judith A. West-Mays, None
  • Footnotes
    Support  NIH EY11910 (JWM); NEI EY 012995 (MLR)
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 2775. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Christine L. Kerr, Mizna Zaveri, Michael L. Robinson, Judith A. West-Mays; Ap-2α Plays Role In Lens Epithelial Cell Maintenance Subsequent To Lens Vesicle Separation. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2775.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose: : The Activating Protein-2 (AP-2) transcription factors are a family of genes playing essential roles in the development of multiple tissues, including the eye. Previous work in our lab has illustrated a cell autonomous role for AP-2α in early lens development. For example, Le-AP-2α mutants with AP-2α conditionally deleted from the lens placode and derivatives displayed a failure in lens separation. Additional work from our lab demonstrated that ectopic expression of AP-2α in the fiber cell region of the lens resulted in expanded expression of E-cadherin and misexpression of Pax6 in newly differentiated fiber cells. In the current study, we investigated the requirement of AP-2α in later stages of lens development, subsequent to lens vesicle separation in order to understand the role of AP-2α in maintenance of the lens epithelium.

Methods: : The MLR10 cre mouse line (in which cre-recombinase is expressed in the lens at E10.5 and later), was crossed with the AP-2αlacZKI/+ mouse line. Pups AP-2αlacZKI/+ and cre positive were crossed with the AP-2αflox/flox mouse line to create a conditional deletion of AP-2α from the lens following its separation from the overlying ectoderm. Eyes and lenses were examined at embryonic and postnatal stages using histological and immunofluorescent techniques.

Results: : Immunostaining for AP-2α indicated its deletion from the lens epithelium at E11.5 and later. A few cells in the epithelium of the mutants at all stages expressed AP-2α positive cells due to the mosaic behaviour of the cre activity. Hematoxylin and Eosin staining between E11.5 and E15.5 did not reveal any morphological abnormalities. However, by E18.5, vacuoles were evident throughout the fiber cell region of the lens, and this defect was greatly attenuated by P4. At P4, pockets of multilayered epithelial cells were also seen in a misshapen mutant lens. Lens epithelial and fiber cell markers Pax6, E-cadherin and β-Crystallin were expressed normally throughout development.

Conclusions: : Our studies of mice with AP-2α conditionally deleted from the lens have revealed a requirement for AP-2α in the lens during later stages, subsequent to lens vesicle separation. These mutants offer a model for the continued examination of the role of AP-2α in maintenance of the lens epithelial phenotype.

Keywords: development • genetics • transcription factors 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×