Unbound MEDLINE

Requirements for Jag1-Rbpj mediated Notch signaling during early mouse lens development.

Abstract

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.

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  • Authors

    Le TT, Conley KW, Mead TJ, Rowan S, Yutzey KE, Brown NL

    Institution

    Division of Developmental Biology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio 45229, USA.

    Source

    Developmental dynamics : an official publication of the American Association of Anatomists 241:3 2012 Mar pg 493-504

    MeSH

    Adaptor Protein Complex 2
    Animals
    Calcium-Binding Proteins
    Gene Deletion
    Heart Defects, Congenital
    Immunoglobulin J Recombination Signal Sequence-Binding Protein
    Integrases
    Intercellular Signaling Peptides and Proteins
    Lens, Crystalline
    Liver
    Membrane Proteins
    Mice
    Mice, Inbred C57BL
    Mice, Inbred Strains
    Receptors, Notch
    Signal Transduction

    Pub Type(s)

    Journal Article
    Research Support, N.I.H., Extramural
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    22275127