Establishment of the neurogenic boundary of the mouse retina requires cooperation of SOX2 and WNT signaling.

ABSTRACT:

Background

Eye development in vertebrates relies on the critical regulation of SOX2 expression. Humans with mutations in SOX2 often suffer from eye defects including anophthalmia (no eye) and microphthalmia (small eye). In mice, deletion of Sox2 in optic cup progenitor cells results in loss of neural competence and cell fate conversion of the neural retina to a non-neurogenic fate, specifically the acquisition of fate associated with progenitors of the ciliary epithelium. This fate is also promoted with constitutive expression of stabilized β-Catenin in the optic cup, where the WNT pathway is up-regulated. We addressed whether SOX2 co-ordinates the neurogenic boundary of the retina through modulating the WNT/β-Catenin pathway by using a genetic approach in the mouse.

Results

SUBMITTER: Heavner WE 

PROVIDER: S-EPMC4295269 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature