Tgfbr2-mutant mice lack corneal expression of the transcription factor Foxc1. (a) In vivo fate mapping at E15 (βGal, blue) demonstrates that NC-derived cells have correctly migrated into control and Tgfbr2-mutant eyes, contributing to corneal stroma and endothelium. (b) At E13.5, the periocular mesenchyme of control eyes is positive for Foxc1 antibody staining (brown; arrowheads), whereas Foxc1 is undetectable in corresponding structures of Tgfbr2-mutant eyes (open arrowheads). (c) No apoptotic cells are found in either control or Tgfbr2-mutant eyes at E13.5 by TUNEL analysis (open arrowheads). (d) At E15, the eyes of control embryos show strong expression of Foxc1 (brown) in the forming trabecular meshwork (arrow) and in corneal endothelial cells (arrowheads). In Tgfbr2-mutant eyes, NC-derived cells localize to the cornea, but Foxc1 is undetectable in prospective endothelial cells (open arrowheads) and in the forming trabecular meshwork (open arrow). (e) At E15, cells that fail to express Foxc1 in Tgfbr2-mutant eyes appear to undergo apoptosis, unlike in control eyes, as revealed by TUNEL analysis (red).
Ittner et al. Journal of Biology 2005 4:11 doi:10.1186/jbiol29