| First Author | Andersson ER | Year | 2010 |
| Journal | Dev Dyn | Volume | 239 |
| Issue | 1 | Pages | 237-45 |
| PubMed ID | 19795512 | Mgi Jnum | J:155226 |
| Mgi Id | MGI:4413372 | Doi | 10.1002/dvdy.22101 |
| Citation | Andersson ER, et al. (2009) Genetic interaction between Lrp6 and Wnt5a during mouse development. Dev Dyn 239(1):237-245 |
| abstractText | 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. |
