PAPC mediates self/non-self-distinction during Snail1-dependent tissue separation.
Bottom Line: First, PAPC attenuates planar cell polarity signaling at the ectoderm-mesoderm boundary to lower cell adhesion and facilitate cleft formation.It consists of short stretches of adherens junction-like contacts inserted between intermediate-sized contacts and large intercellular gaps.These roles of PAPC constitute a self/non-self-recognition mechanism that determines the site of boundary formation at the interface between PAPC-expressing and -nonexpressing cells.
Affiliation: Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada M5S 3G5.Show MeSH
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Mentions: To analyze downstream effects of PAPC/Snail1 during tissue separation, we explored a seemingly paradoxical finding: Dvl2 was required for Xsnail1 expression, but Dvl2-MO did not block separation behavior (Fig. 5 A). One possibility is that Dvl2-MO inhibited Xsnail1 expression but rescued separation further downstream; indeed, Dvl2-MO rescued separation in Xsnail1-MO–injected as well as PTX-treated mesoderm (Fig. 5 A). The PCP component Prickle (Pk1) is up-regulated in Xenopus mesoderm (Takeuchi et al., 2003; Veeman et al., 2003) and in the axial mesoderm of zebrafish (Carreira-Barbosa et al., 2003). Pk1 knockdown, which neither blocked separation (Fig. 5 A) nor reduced Xsnail1 expression (Fig. S5 A), also rescued separation. The PCP component Vangl2/Stbm had similar effects (Fig. 5 A). In the zebrafish, Dvl2-MO and Pk-MO likewise rescued tissue separation (Fig. 5 B and Fig. S1 H).
Affiliation: Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada M5S 3G5.