Abstract
Abstract: :
Purpose: Ocular glands in mice, Harderian and lacrimal glands, are induced from nasal and temporal sides of conjunctival epithelium, respectively, by epithelial-mesenchymal interactions. Gli family proteins (Gli1, 2 and 3) are the transcription factors with zinc finger domain functioning mainly at the downstream of the Sonic hedgehog (Shh) signal pathway, regulating induction of various organs. Gli3 mutant mice known as Extra-toes have multiple abnormalities including CNS defect and polydactyly. In this study, we have analyzed Gli3 mutant mice to examine the functions of Gli family proteins in the development of ocular glands. Methods: To obtain homozygous mutant embryos of Extra-toes, we crossed male and female heterozygotes. Paraffin sections of ocular tissues of homozygous and wild type embryos from E13.5 to E17.5 were stained with Hematoxylin and Eosin. Whole-mount and section in situ hybridization was performed to visualize Gli1-3 and other genes. Results: Homozygotes of Gli3 mutant embryos were mostly microphtalmic and lacrimal glands were absent, while Harderian glands were normal. Though the migration of lacrimal mesenchymal tissue and expression of Fgf10, an inducer of the gland, in it was normal. The expression of Fgfr2IIIb, however, was weaker than that in the epithelium of nasal side. Conclusions:These results above suggest that Gli3 is involving in proliferation of conjunctival epithelium on temporal side and is essential for the development of lacrimal gland but not for Harderian gland, implying that other Gli member(s) might have redundant functions in the development of Harderian gland.
Keywords: lacrimal gland • gene/expression