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Requirements for Jag1‐Rbpj mediated Notch signaling during early mouse lens development
Author(s) -
Le Tien T.,
Conley Kevin W.,
Mead Timothy J.,
Rowan Sheldon,
Yutzey Katherine E.,
Brown Nadean L.
Publication year - 2012
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.23739
Subject(s) - jag1 , notch signaling pathway , optic vesicle , biology , microbiology and biotechnology , lens (geology) , morphogenesis , eye development , ectoderm , endoderm , lens fiber , anatomy , embryogenesis , embryonic stem cell , signal transduction , embryo , genetics , transcription factor , gene , nucleus , paleontology
Background: During vertebrate lens development, the lens placode in the embryonic ectoderm invaginates into a lens vesicle, which then separates from the surface epithelium, followed by two waves of fiber cell differentiation. In the mouse, multiple labs have shown that Jag1‐Notch signaling is critically required during the second wave of lens fiber cell formation. However, Notch signaling appears to play no obvious role during lens induction or morphogenesis, although multiple pathway genes are expressed at these earlier stages. Results: Here, we explored functions for Notch signaling specifically during early lens development, by using the early‐acting AP2α‐Cre driver to delete Jag1 or Rbpj . We found that Jag1 and Rbpj are not required during lens induction, but are necessary for proper lens vesicle separation from the surface ectoderm. Conclusions: We conclude that precise levels of Notch signaling are essential during lens vesicle morphogenesis. In addition, AP2α‐Cre‐mediated deletion of Rbpj resulted in embryos with cardiac outflow tract and liver deformities, and perinatal lethality. Developmental Dynamics 241:493–504, 2012. © 2012 Wiley Periodicals, Inc.