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. Author manuscript; available in PMC: 2010 Feb 26.
Published in final edited form as: Development. 2008 Jan 16;135(4):717–727. doi: 10.1242/dev.015339

Fig. 5. Wnt-β-catenin signaling synergizes with that of PPARδ to confer blastocyst competency for implantation.

Fig. 5

(A, B) Overexpressing levels of DKK1 or PKF115-584 blocked activation of dormant blastocysts for implantation in response to E2 (3 ng/mouse). Numbers within the bar indicate the number of mice with implantation sites (IS)/total number of mice examined. (C, D) Representative photomicrographs of uteri without blue bands and morphologically dormant blastocysts recovered from mice treated with PKF115-584 (Bar, 50 μm). (E, F) Recombinant Wnt3a protein (200 ng/ml) induced nuclear stabilization of active dephospho β-catenin and PPARδ expression in dormant blastocysts in culture. Cotreatment of Wnt3a with DKK1 (1 μg/ml) or PKF115-584 (1 μM) antagonized Wnt3a-induced β-catenin stabilization. Images shown depict Cy3-labeled antigens as red, SYTO-13-labeled nuclei as green and merge as yellow. Bar, 50 μm. (G, H) Wnt3a and/or GW501516 conferred blastocyst implantation competency. Dormant blastocysts were cultured in the presence of vehicle, Wnt3a (200 ng/ml) and/or GW501516 (a selective PPARδ agonist, 1 μM) for 24h before transferred into pseudopregnant delayed recipients. Numbers within the bar in G indicate the number of recipients with IS/total number of mice examined, and those in H indicate the number of IS/total number of blastocysts transferred.

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