Journal
DEVELOPMENTAL DYNAMICS
Volume 233, Issue 2, Pages 368-372Publisher
WILEY
DOI: 10.1002/dvdy.20437
Keywords
limb development; Wnt signaling; Lrp6; Wnt7a
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Funding
- NIGMS NIH HHS [GM24872] Funding Source: Medline
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Wnt7a and the Wnt coreceptor Lrp6 are both required for development of posterior digits and dorsal structures of the limb. We report that Lrp6 null mice lack Lmx1b expression in the distal mesenchyme, as previously described for Wnt7a mutants. The loss of Lmx1b expression in Wnt7a(-/-)Lrp6(+/-) double mutants did not differ from that in Wnt7a(-/-) mice. These data suggest that Wnt7a acts through Lrp6 to regulate Lmx1b expression during dorsal specification. The loss of posterior skeletal elements in the Wnt7a(-/-)Lrp6(+/-) double mutant was much more severe than in Wnt7a(-/-) mice, suggesting that the Wnt7a(-/-) limb is protected by the action of other Lrp6 ligands. The data are consistent with the view that Wnt7a acts through Lrp6 and the canonical Wnt signaling pathway during dorsal and posterior limb development in the mouse. (c) 2005 Wiley-Liss, Inc.
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