Combinatorial regulation of optic cup progenitor cell fate by SOX2 and PAX6 | Zendy

Danielle Matsushima | Zendy; Whitney E. Heavner | Zendy; Larysa Pevny | Zendy

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Combinatorial regulation of optic cup progenitor cell fate by SOX2 and PAX6

Author(s) -

Danielle Matsushima,

Whitney E. Heavner,

Larysa Pevny

Publication year - 2011

Publication title -

development

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.15

H-Index - 36

eISSN - 1477-9129

pISSN - 0950-1991

DOI - 10.1242/dev.055178

Subject(s) - pax6 , biology , haploinsufficiency , sox2 , anophthalmia , microphthalmia , microbiology and biotechnology , aniridia , progenitor , progenitor cell , neural stem cell , axon guidance , genetics , phenotype , stem cell , embryonic stem cell , transcription factor , gene , axon

In humans, haploinsufficiency of either SOX2 or PAX6 is associated with microphthalmia, anophthalmia or aniridia. In this study, through the genetic spatiotemporal specific ablation of SOX2 on both wild-type and Pax6-haploinsufficent backgrounds in the mouse, we have uncovered a transcriptionally distinct and developmentally transient stage of eye development. We show that genetic ablation of SOX2 in the optic cup results in complete loss of neural competence and eventual cell fate conversion to non-neurogenic ciliary epithelium. This cell fate conversion is associated with a striking increase in PAX6, and genetically ablating SOX2 on a Pax6-haploinsufficient background partially rescues the Sox2-mutant phenotype. Collectively, these results demonstrate that precise regulation of the ratio of SOX2 to PAX6 is necessary to ensure accurate progenitor cell specification, and place SOX2 as a decisive factor of neural competence in the retina.

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