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E.A. Bassett, K. Chan, T. Marquardt, T. Williams, J.A. West–Mays; Deletion of Amacrine Cell Marker AP–2 Results in No Overt Amacrine Cell Defects . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2779.
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We have previously shown that transcription factor AP–2α has specific roles in development of the lens and cornea. AP–2α is also expressed in the developing retina and AP–2α null mice exhibit defects in the developing optic cup; however, the retinal expression of this protein and its possible role in retinogenesis have not been investigated in detail. To this end, we have analyzed the temporal and spatial expression patterns of AP–2α, and created a conditional deletion of AP–2α in the developing retina.
Throughout retinogenesis, immunofluoresence was used to perform colocalizations of AP–2α and various markers of retinal cell types and cell proliferation. The Cre–loxP system was used to create ‘Ret–AP–2α’ mutants with a conditional deletion of AP–2α in the developing retina. Retina–specific deletion of AP–2α was confirmed, and mutants were histologically compared to their control littermates.
The AP–2α protein was initially detected in the central retina at E13.5, and was distinctly expressed throughout development and adulthood, first in the presumptive inner nuclear layer (INL) and later in both the INL and ganglion cell layer (GCL). AP–2α did not colocalize with the mitosis marker phospho–histone H3 or the ganglion cell marker Brn3b at any embryonic or postnatal stages, but did colocalize with the amacrine cell markers calretinin and glycine transporter 1. Like their control littermates, the retinas of Ret–AP–2α mutants were fully laminated, with no overt defects observed by histological examination or staining patterns of syntaxin, glycine transporter 1 or calretinin. Ret–AP–2α mutants did not exhibit the duplicated neuroretina and loss of retinal pigmented epithelium (RPE) observed previously in full AP–2α null mice.
AP–2α was shown to be an early marker of post–mitotic amacrine transition cells in the embryonic retina, as well as differentiated amacrine cells in the mature retina. The lack of phenotypic defects in Ret–AP–2α mutants suggests that AP–2ß, a closely related family member that is also expressed in the developing retina, may be playing a compensatory role. Failure to observe the loss of RPE present in full AP–2α null mice suggests that this defect may be caused by the absence of AP–2α in other tissues (ex. the neural crest) contributing to the developing eye. A conditional deletion of both AP–2α and ß will provide a model for examining the possible co–operative or redundant roles of these family members in retinogenesis.
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