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Diverse dependencies of developing Merkel innervation on the trkA and both full-length and truncated isoforms of trkC

  1. Author:
    Cronk, K. M.
    Wilkinson, G. A.
    Grimes, R.
    Wheeler, E. F.
    Jhaveri, S.
    Fundin, B. T.
    Silos-Santiago, I.
    Tessarollo, L.
    Reichardt, L. F.
    Rice, F. L.
  2. Author Address

    Albany Med Coll, Ctr Neuropharmacol & Neurosci, Albany, NY 12208 USA Albany Med Coll, Ctr Neuropharmacol & Neurosci, Albany, NY 12208 USA Univ Calif San Francisco, Howard Hughes Med Ctr, Neurosci Unit, San Francisco, CA 94143 USA Univ Texas, Div Life Sci, San Antonio, TX 78249 USA MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA Astra Zeneca R&D Sodertalje, Dept Mol Sci, SE-14157 Huddinge, Sweden Millennium Pharmaceut Inc, Dept Neurobiol, Cambridge, MA 02139 USA NCI, FCRDC, Neural Dev Grp, Frederick, MD 21702 USA Rice FL Albany Med Coll, Ctr Neuropharmacol & Neurosci, Albany, NY 12208 USA
    1. Year: 2002
  1. Journal: Development
    1. 129
    2. 15
    3. Pages: 3739-3750
  2. Type of Article: Article
  1. Abstract:

    This study demonstrates that innervation dependent on two different neurotrophin tyrosine kinase (trk) receptors can form the same types of sensory endings (Merkel endings) in the same target (Merkel cells of vibrissa follicles). Some endings transiently express trkA during their initial development, whereas others express trkC throughout their development. Consequently, elimination of kinase domains of either trkA or trkC each result in a partial loss of Merkel endings, whereas absence of kinase domains of both receptors results in a total loss. At the onset of Merkel ending development, at least one kinase-lacking trkC isoform is transiently expressed on all the follicle cells, while neurotrophin 3 is transiently expressed only in the cells at the middle third of the follicle where the Merkel endings and cells develop. This transient non-neuronal expression of truncated trkC is essential for development of any Merkel endings, whereas some Merkel endings and cells still begin to develop in the absence of neurotrophin 3. Therefore, truncated trkC plays a more important role in the development of this innervation than kinase forms of trkA or trkC or of NT3, the only known ligand for trkC receptors.

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