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Canonical Wnt signaling is required for ophthalmic trigeminal placode cell fate determination and maintenance.

Canonical Wnt signaling is required for ophthalmic trigeminal placode cell fate determination and maintenance. Research Abstract Details 

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  • Canonical Wnt signaling is required for ophthalmic trigeminal placode cell fate determination and maintenance. Abstract Text:

    rhonda n t lassiterRhonda N T Lassiter,carolynn m dudeCarolynn M Dude,stephanie b reynoldsStephanie B Reynolds,nichelle i wintersNichelle I Winters,clare v h bakerClare V H Baker,michael r starkMichael R Stark,

    Cranial placodes are ectodermal regions that contribute extensively to the vertebrate peripheral sensory nervous system. The development of the ophthalmic trigeminal (opV) placode, which gives rise only to sensory neurons of the ophthalmic lobe of the trigeminal ganglion, is a useful model of sensory neuron development. While key differentiation processes have been characterized at the tissue and cellular levels, the signaling pathways governing opV placode development have not. Here we tested in chick whether the canonical Wnt signaling pathway regulates opV placode development. By introducing a Wnt reporter into embryonic chick head ectoderm, we show that the canonical pathway is active in Pax3+ opV placode cells as, or shortly after, they are induced to express Pax3. Blocking the canonical Wnt pathway resulted in the failure of targeted cells to adopt or maintain an opV fate, as assayed by the expression of various markers including Pax3, FGFR4, Eya2, and the neuronal differentiation markers Islet1, neurofilament, and NeuN, although, surprisingly, it led to upregulation of Neurogenin2, both in the opV placode and elsewhere in the ectoderm. Activating the canonical Wnt signaling pathway, however, was not sufficient to induce Pax3, the earliest specific marker of the opV placode. We conclude that canonical Wnt signaling is necessary for normal opV placode development, and propose that other molecular cues are required in addition to Wnt signaling to promote cells toward an opV placode fate.

    Canonical Wnt signaling is required for ophthalmic trigeminal placode cell fate determination and maintenance. Publishing Authors By Initials

    rn lassiterRN Lassiter,cm dudeCM Dude,sb reynoldsSB Reynolds,ni wintersNI Winters,cv bakerCV Baker,mr starkMR Stark,

    For similar peptides: intercellular signaling peptides and proteins: wnt proteins research abstracts see: peptides: intercellular signaling peptides and proteins: wnt proteins research

    PUBMED ID PMID:

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    Canonical Wnt signaling is required for ophthalmic trigeminal placode cell fate determination and maintenance. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Developmental biology

    VOLUME: 308

    Page Numbers: 392-406

    Journal Abbreviation: Dev. Biol.

    ISSN: 0012-1606

    DAY: 2

    MONTH: 06

    YEAR: 2007

    Canonical Wnt signaling is required for ophthalmic trigeminal placode cell fate determination and maintenance. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 372762

    Canonical Wnt signaling is required for ophthalmic trigeminal placode cell fate determination and maintenance. Keywords Mesh Terms:

    KEYWORDS: Wnt Proteins

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Canonical Wnt signaling is required for ophthalmic trigeminal placode cell fate determination and maintenance. Information

    Substance Name: Wnt Proteins

    Registry Number: 0

    Grant and Affiliation Information for Canonical Wnt signaling is required for ophthalmic trigeminal placode cell fate determination and maintenance.

    AFFILIATION: Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84663, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NICHD

    GRANT: 5R03HD041470-02

    ACRONYM: HD

    MEDLINETA: Dev Biol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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