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Keely M. Bumsted, Colin J. Barnstable; Dorsal Retinal Pigment Epithelium Differentiates as Neural Retina in the Microphthalmia (mi/mi) Mouse. Invest. Ophthalmol. Vis. Sci. 2000;41(3):903-908.
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purpose. Microphthalmia, a bHLH-zip transcription factor associated
with the onset and maintenance of pigmentation, identifies the retinal
pigment epithelial (RPE) compartment during optic vesicle and optic cup
development. To determine a role for microphthalmia (mi) during eye development, the effects of an mi loss of function mutation on RPE and neural retinal
were investigated in the mi/mi mouse.
methods. A series of embryonic and postnatal mi/mi and wild-type
eyes were sectioned and labeled with neural retina– and RPE cell
type–specific antibodies. Photoreceptor loss was quantified by
counting the number of photoreceptor nuclei spanning the outer nuclear
layer throughout postnatal retinal development.
results. Early neural retinal differentiation is not affected in the mi/mi mouse. The mi/mi ventral retinal
pigment epithelial layer begins to develop normally, but does not
pigment or attain a differentiated cuboidal morphology. The dorsal
region of mi/mi retinal pigment epithelium expands and
forms an ectopic retina, which develops all major retinal cell types
along a similar time course as the wild type. After birth, mi/mi photoreceptors begin to form rosettes, outer
segments fail to elongate, and over an extended time period, the retina
conclusions. Together these results suggest that early retinal development can
proceed normally in the mi/mi mutant, but later retinal
histogenesis is dependent on the presence of a differentiated retinal
pigment epithelium. Most importantly, loss of mi function permits a change in cell fate from RPE to retina in the dorsal
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