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: PCP signaling has been implicated in cell adhesion (see Discussion). When we knocked down Dvl2 or Pk1 in mesoderm explants or in the embryo, cell separation generated pronounced retraction fibers (Fig. 6, A–F), reminiscent of the membrane tethers between detaching mesoderm and BCR cells at Brachet’s cleft (Rohani et al., 2011). In addition, tissue surface tension, a measure of cell adhesion, was diminished in the mesoderm by Pk1-MO (Fig. 6 G), and Pk1-MO–injected cells showed reduced mixing with uninjected cells (Fig. 6 H). In contrast, injection of ephrinB1-MO increased surface tension (Fig. 6 G), consistent with Eph/ephrin signaling normally lowering mesoderm cohesion (Rohani et al., 2014). We propose that PCP puncta strengthen adhesion within the mesoderm to counteract the effects of Eph/ephrin and that their down-regulation at the mesoderm–ectoderm boundary permits tissue separation. Removal of Dvl puncta from the boundary-apposed membranes of cells, but not from interior membranes, is compatible with the simultaneous requirement for Dvl2 in Snail1 expression. Its role as an EphB-interacting protein (Tanaka et al., 2003) in the context of tissue separation remains to be elucidated.
Affiliation: Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada M5S 3G5.