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Significance Blastocyst implantation is a complex process that coordinates reciprocal embryo–uterine interactions. The uterus is demarcated by mesometrial (A)–antimesometrial (AM) domains; implantation occurs at regularly spaced intervals along the longitudinal axis of the AM pole, within specialized implantation chambers (crypts). The organized crypt formation in the rodent uterus was first observed in 1901, but the mechanism driving this phenomenon remained unknown. We found that planar cell polarity (PCP) signaling coordinates luminal epithelial evaginations toward the AM domain to form crypts for embryo homing and implantation in mice. Disruption of PCP signaling by inactivation of Vang-like protein 2, but not Vang-like protein 1, in the uterus disturbs the regular formation of epithelial evaginations and crypts, disrupting implantation and decidualization and severely compromising pregnancy outcomes.

Planar cell polarity signaling in the uterus directs appropriate positioning of the crypt for embryo implantation