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The formation of multiple pituitary pouches from the oral ectoderm causes ectopic lens development in hedgehog signaling‐defective avian embryos
Author(s) -
Taira Yuki,
Ikuta Yuya,
Inamori Sachiko,
Nunome Mitsuo,
Nakano Mikiharu,
Suzuki Takayuki,
Matsuda Yoichi,
Tsudzuki Masaoki,
Teramoto Machiko,
Iida Hideaki,
Kondoh Hisato
Publication year - 2020
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.222
Subject(s) - biology , ectoderm , embryo , microbiology and biotechnology , hedgehog , embryogenesis , anatomy , eye development , hedgehog signaling pathway , signal transduction , genetics , gene , phenotype
Background Hedgehog signaling has various regulatory functions in tissue morphogenesis and differentiation. To investigate its involvement in anterior pituitary precursor development and the lens precursor potential for anterior pituitary precursors, we investigated Talpid mutant Japanese quail embryos, in which hedgehog signaling is defective. Results Talpid mutants develop multiple pituitary precursor‐like pouches of variable sizes from the oral ectoderm (OE). The ectopic pituitary pouches initially express the pituitary‐associated transcription factor (TF) LHX3 similarly to Rathke's pouch, the genuine pituitary precursor. The pouches coexpress the TFs SOX2 and PAX6, a signature of lens developmental potential. Most Talpid mutant pituitary pouches downregulate LHX3 expression and activate the lens‐essential TF PROX1, leading to the development of small lens tissue expressing α‐, β‐, and δ‐crystallins. In contrast, mutant Rathke's pouches express a lower level of LHX3, which is primarily localized in the cytoplasm, and activate the lens developmental pathway. Conclusions Hedgehog signaling in normal embryos regulates the development of Rathke's pouch in two steps. First, by confining Rathke's pouch development in a low hedgehog signaling region of the OE. Second, by sustaining LHX3 activity to promote anterior pituitary development, while inhibiting ectopic lens development.