April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Latent Lens Phenotype in Mice Lacking Eph-receptor A2
Author Affiliations & Notes
  • Steven Bassnett
    Ophthal & Vis Science, Washington Univ Sch of Med, Saint Louis, Missouri
  • Yanrong Shi
    Ophthal & Vis Science, Washington Univ Sch of Med, Saint Louis, Missouri
  • Alicia De Maria
    Ophthal & Vis Science, Washington Univ Sch of Med, Saint Louis, Missouri
  • Jennifer King-Sitzes
    Ophthal & Vis Science, Washington Univ Sch of Med, Saint Louis, Missouri
  • Thomas Bennett
    Ophthal & Vis Science, Washington Univ Sch of Med, Saint Louis, Missouri
  • Alan Shiels
    Ophthal & Vis Science, Washington Univ Sch of Med, Saint Louis, Missouri
  • Footnotes
    Commercial Relationships  Steven Bassnett, None; Yanrong Shi, None; Alicia De Maria, None; Jennifer King-Sitzes, None; Thomas Bennett, None; Alan Shiels, None
  • Footnotes
    Support  NIH/NEI grants EY12284, EY09852, EY018185, EY02687 and RPB
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4774. doi:
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    • Get Citation

      Steven Bassnett, Yanrong Shi, Alicia De Maria, Jennifer King-Sitzes, Thomas Bennett, Alan Shiels; Latent Lens Phenotype in Mice Lacking Eph-receptor A2. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4774.

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

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Abstract

Purpose: : Variations in the gene coding for ephrin type-A receptor-2 (EphA2) have been associated with a cataract phenotype in humans and mice. Here we characterize the lens phenotype of Epha2 gene-targeted mice that do not develop obvious cataract.

Methods: : Commercially available Epha2-targeted mice were characterized by standard PCR-amplification and sequencing techniques. Lenses were analyzed by immuno-blotting, bright-field microscopy, and confocal fluorescence microscopy techniques.

Results: : DNA/RNA amplification and sequencing confirmed that the Epha2 gene was disrupted in exon-5 resulting in several mutant transcripts consistent with a functional null at the protein level. Lens immunoblot analysis and confocal immunofluorescence microscopy localized Epha2 to plasma-membranes of the anterior epithelium and peripheral cortical fibers of wild-type but not null mice. Bright-field microscopy showed that Epha2-null lenses were smaller than wild-type and, while transparent, displayed a mild central refractive disturbance. Confocal fluorescence imaging of live Epha2-null lenses revealed at least four other features not observed in wild-type: (1) anterior and posterior Y-sutures were offset from the optical axis and composed of 1-5 asymmetric branches, (2) fiber cell nuclei at the lens equator appeared disorganized and were retained with age, (3) isolated fiber cells lacked characteristic undulation along their anterior-posterior axis, and (4) membranous dome-like structures protruded from the basal surface of the anterior epithelium into the surrounding capsule.

Conclusions: : Homozygous loss of Epha2 affects lens growth and optical quality, but is not necessarily sufficient to cause cataract in mice. Absence of Epha2 is also associated with mis-targeting of fiber cells to the suture regions, abnormal fiber cell shape and denucleation, and aberrant basal protrusions from the anterior epithelium. These data point to a key role for Epha2-dependent cell signaling in normal lens development.

Keywords: microscopy: confocal/tunneling • cell membrane/membrane specializations • differentiation 
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