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¹ Division of Developmental Neuroscience, Center for Translational and Advanced Animal Research, Tohoku University Graduate School of Medicine, 2-1, Seiryo-machi, Aoba-ku, Sendai, 980-8575, Japan
² Department of Ophthalmology, Tohoku University Graduate School of Medicine, 1-1, Seiryo-machi, Aoba-ku, Sendai, 980-8575, Japan
³ Division of Developmental Genetics, Institute of Molecular Embryology and Genetics, Kumamoto University, 4-24-1, Kuhonji, Kumamoto, 862-0976, Japan
⁴ Division of Stem Cell Regulation Research, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan
⁵ CREST Japan Science and Technology Agency, 4-1-8, Honcho, Kawaguchi, 332-0012 Japan

PAX6/Pax6 gene encodes a transcription factor that is crucially required for eye development. Pax6 heterozygous mutant mouse (Pax6^Sey/+) shows various ocular defects, especially in the anterior segment. It has been well known that the induction of the lens and development of the cornea and retina are dependent on PAX6/Pax6 in a cell-autonomous fashion, although the influence of PAX6/Pax6 on the other tissues derived from the ocular mesenchyme is largely unknown. Using transgenic mouse lines in which neural crest cells are genetically marked by LacZ or EGFP, we revealed the extensive contribution of neural crest derived cells (NCDCs) to the ocular tissues. Furthermore, various eye defects in Pax6^Sey/+ mouse were accompanied by abnormal distribution of NCDCs from early developmental stages to the adult. In Pax6^Sey/+ mouse mice, neural crest cells abnormally migrated into the developing eye in a cell nonautonomous manner at early embryonic stages. These results indicate that normal distribution and integration of NCDCs in ocular tissues depend on a proper dosage of Pax6, and that Pax6^Sey/+ eye anomalies are caused by cell autonomous and nonautonomous defects due to Pax6 haploinsufficiency.

^* Correspondence: E-mail: osumi{at}mail.tains.tohoku.ac.jp

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