Epithelial SOX11 regulates eyelid closure during embryonic eye development

Biochem Biophys Res Commun. 2021 Apr 16:549:27-33. doi: 10.1016/j.bbrc.2021.02.075. Epub 2021 Mar 1.

Abstract

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.

Keywords: Corneal opacity; Eyelid open at birth; SOX11; c-Jun.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Aging / pathology
  • Animals
  • Cornea / pathology
  • Embryo, Mammalian / pathology
  • Embryonic Development*
  • Epithelial Cells / metabolism*
  • Eyelids / embryology*
  • Eyelids / metabolism*
  • Inflammation / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mutation / genetics
  • Proto-Oncogene Proteins c-jun / metabolism
  • SOXC Transcription Factors / genetics
  • SOXC Transcription Factors / metabolism*

Substances

  • Actins
  • Proto-Oncogene Proteins c-jun
  • SOXC Transcription Factors
  • Sox11 protein, mouse