Journal
DEVELOPMENTAL BIOLOGY
Volume 279, Issue 2, Pages 308-321Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2004.12.018
Keywords
retina; mouse embryo; mutant; sey; small eye; aniridia; transcription factor; neurogenesis; neuron differentiation; proneural; bHLH; mash1; Bm3b; Isll; timing
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Funding
- NEI NIH HHS [R01 EY13612, R01 EY013612, R01 EY013612-04] Funding Source: Medline
- NICHD NIH HHS [R01 HD38069, R01 HD038069] Funding Source: Medline
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The transcription factor Pax6 plays a pivotal role in eye development, as eye morphogenesis is arrested at a primitive optic vesicle stage in homozygous Pax6 mutant mouse embryos. The arrested optic vesicle development has led to the assumption that cellular differentiation programs are unable to initiate. Contrary to this, we found that neurogenesis in Pax6 mutant optic vesicles was not arrested, but instead accelerated as numerous neurons differentiated precociously, more than a day earlier than normal. To identify potential mechanisms for Pax6 repression of neuron differentiation, we examined retinal proliferation and differentiation. Mutant optic vesicles had reduced proliferation, coupled with precocious activation of the proneural gene, Mash 1. Ectopic expression of Mash 1 was sufficient to induce precocious neuron differentiation. Subsequently, precocious neurons adopted a generic rather than a specific retinal neuron fate. Thus, Pax6 regulates the timing of retinal neurogenesis and couples it with specific neuron differentiation programs. (C) 2004 Elsevier Inc. All rights reserved.
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