Epithelial SOX11 regulates eyelid closure during embryonic eye development

Fibroblast growth factor (FGF10)-mediated signals are essential for embryonic eyelid closure in mammals. Systemic SOX11-deficient mice are born with unclosed eyelids, suggesting a possible role of SOX11 in eyelid closure. However, the underlying mechanisms of this process remain unclear. In this study, we show that epithelial deficiency of SOX11 causes a defect in the extension of the leading edge of the eyelid, leading to failure of embryonic eyelid closure. c-Jun in the eyelid is a transcription factor downstream of FGF10 required for the extension of the leading edge of the eyelid, and c-Jun level was decreased in epithelial SOX11-deficient embryos. These results suggest that epithelial SOX11 plays an important role in embryonic eyelid closure. ? 2021 Elsevier Inc. All rights reserved.

Automated summary

SOX11 deficiency in epithelial cells impairs the extension of the leading edge of eyelids, resulting in embryonic eyelid closure failure. The transcription factor c-Jun downstream of FGF10 is required for this extension and its levels are decreased in SOX11-deficient embryos.