Zebrafish mutations in Gli-mediated hedgehog signaling lead to lens transdifferentiation from the adenohypophysis anlage
- Kondoh, H., Uchikawa, M., Yoda, H., Takeda, H., Furutani-Seiki, M., and Karlstrom, R.O.
- Mechanisms of Development 96(2): 165-174 (Journal)
- Registered Authors
- Furutani-Seiki, Makoto, Karlstrom, Rolf, Kondoh, Hisato, Takeda, Hiroyuki
- transdifferentiation; adonohypophysis; lens; crystallins; zebrafish; midline mutants; you-too; iguana; Gli2; Rathke's pouch; talpid(3)
- MeSH Terms
- Chick Embryo
- Hedgehog Proteins
- In Situ Hybridization
- Lens, Crystalline/embryology*
- Lens, Crystalline/metabolism
- Oncogene Proteins/genetics
- Pituitary Gland, Anterior/embryology*
- Pituitary Gland, Anterior/metabolism
- Signal Transduction
- Species Specificity
- Transcription Factors/genetics
- Zebrafish Proteins*
- 10960781 Full text @ Mech. Dev.
Kondoh, H., Uchikawa, M., Yoda, H., Takeda, H., Furutani-Seiki, M., and Karlstrom, R.O. (2000) Zebrafish mutations in Gli-mediated hedgehog signaling lead to lens transdifferentiation from the adenohypophysis anlage. Mechanisms of Development. 96(2):165-174.
It is known that the earliest lens marker delta-crystallin is expressed abundantly in Rathke's pouch of the chicken, suggesting a close relationship between the cell states of the adenohypophysis (pituitary) anlage and the early lens. We show here that the zebrafish midline mutants you-too (yot) and iguana (igu) develop lenses from the adenohypophysis anlage. The early adenohypophysis anlage of normal zebrafish expresses lim3 and six3 but in yot(ty119) mutants the anterior part of the anlage lacks lim3 expression, and instead produces a crystallin-expressing cell population which develops into a large lens structure expressing beta and gamma-crystallins, but is not associated with retina tissues. Among the zebrafish mutants with midline defects, midline lenses were observed in two mutant alleles of yot and an allele of igu, but not in other mutants (syu, con, smh, dtr, uml, spi and lok). Two yot mutant alleles with midline lenses likely encode dominant negative forms of the Gli2 protein which will interfere with transcriptional activation by other Gli proteins. The observation argues that overall inhibition of Shh-Gli signaling leads the adenohypophysis anlage to transdifferentiate into lens.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes