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Genetic Interaction Between Lrp6 and Wnt5a During Mouse Development

  1. Author:
    Andersson, E.
    Bryjova, L.
    Biris, K.
    Yamaguchi, T. P.
    Arenas, E.
    Bryja, V.

  2. Author Address

    [Bryjova, Lenka; Bryja, Vitezslav] Masaryk Univ, Fac Sci, Inst Expt Biol, CS-61137 Brno, Czech Republic. [Bryjova, Lenka; Bryja, Vitezslav] Acad Sci Czech Republic, Inst Biophys, Dept Cytokinet, CS-61265 Brno, Czech Republic. [Andersson, Emma; Bryjova, Lenka; Arenas, Ernest; Bryja, Vitezslav] Karolinska Inst, Dept Med Biochem & Biophys, Stockholm, Sweden. [Biris, Kristin; Yamaguchi, Terry P.] NCI, Canc & Dev Biol Lab, Ctr Canc Res, NIH, Frederick, MD 21701 USA.;Bryja, V, Masaryk Univ, Fac Sci, Inst Expt Biol, Kotlarska 2, CS-61137 Brno, Czech Republic.;Ernest.Arenas@ki.se bryja@sci.muni.cz
    1. Year: 2010
    2. Date: Jan
  2. Journal: Developmental Dynamics
    1. 239
    2. 1
    3. Pages: 237-245
  4. Type of Article: Article
  5. ISSN: 1058-8388
  1. Abstract:

    Lrp6 is generally described as a receptor required for signal transduction in the Wnt/beta-catenin pathway. Wnt5a, however, is a Wnt ligand that usually does not activate Wnt/beta-catenin but rather activates noncanonical Wnt signaling. We have previously shown that Lrp6 can inhibit noncanonical Wnt5a/Wnt11 signaling and that Lrp5/6 loss-of-function produces noncanonical gain-of function defects, which can be rescued by loss of Wnt5a. Here, we describe other phenotypes found in Wnt5a/Lrp6 compound mutant mice, including a worsening of individual Wnt5a or Lrp6 loss of function phenotypes. Lrp6 haploinsufficiency in a Wnt5a-/- background caused spina bifida and exacerbated posterior truncation. Wnt5a-/-Lrp6-/-embryos displayed presomitic mesoderm morphogenesis, somitogenesis, and neurogenesis defects, which are much more severe than in either of the single mutants. Interestingly these results reveal a further level of complexity in processes in which Wnt5a and LRP6 cooperate, or oppose each other, during mouse development. Developmental Dynamics 239:237-245, 2010. Published 2009 Wiley-Liss, Inc.(dagger)

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External Sources

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  2. DOI: 10.1002/dvdy.22101
  3. View record in Web of Science®
  4. WOS: 000273703900021

Library Notes

  1. Fiscal Year: FY2009-2010
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