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PAPC mediates self/non-self-distinction during Snail1-dependent tissue separation.

Luu O, Damm EW, Parent SE, Barua D, Smith TH, Wen JW, Lepage SE, Nagel M, Ibrahim-Gawel H, Huang Y, Bruce AE, Winklbauer R - J. Cell Biol. (2015)

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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada M5S 3G5.

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PAPC function beyond PCP inhibition is required for cleft formation. (A) Quantitation of separation in gain-of-function experiment. BCR was injected as indicated. (B–D) Ectopic cleft formation in the BCR, as in Fig. 3 (G–L). (E) Exemplary kymographs of cleft contact formation, as in Fig. 4 E. (F) Frequency of cleft contacts after reaggregation, as in Fig. 4 C. (G) Reduced Dvl-GFP puncta in EphB4-MO–injected mesoderm (green) at boundary to BCR (red, membrane-RFP in ectoderm). (H) Quantitation of separation behavior. (left) Mesoderm injected as indicated was tested on normal BCR. (right) BCR explants injected as indicated were tested on normal BCR. (I) Model of tissue separation at the mesoderm–ectoderm (BCR) boundary.
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fig7: PAPC function beyond PCP inhibition is required for cleft formation. (A) Quantitation of separation in gain-of-function experiment. BCR was injected as indicated. (B–D) Ectopic cleft formation in the BCR, as in Fig. 3 (G–L). (E) Exemplary kymographs of cleft contact formation, as in Fig. 4 E. (F) Frequency of cleft contacts after reaggregation, as in Fig. 4 C. (G) Reduced Dvl-GFP puncta in EphB4-MO–injected mesoderm (green) at boundary to BCR (red, membrane-RFP in ectoderm). (H) Quantitation of separation behavior. (left) Mesoderm injected as indicated was tested on normal BCR. (right) BCR explants injected as indicated were tested on normal BCR. (I) Model of tissue separation at the mesoderm–ectoderm (BCR) boundary.

Mentions: PCP inhibition is not sufficient for boundary formation. In gain-of-function experiments, coinjection of Dvl2-MO and PAPC, but not Dvl2-MO alone, induced separation (Fig. 7 A). Moreover, when Dvl2-MO was expressed in half of the BCR, no boundary formed, but a cleft appeared when PAPC was coexpressed; the boundary vanished when PAPC was simultaneously expressed in the other half of the BCR (Fig. 7, B–D). These results confirm that Xsnail1 can be functionally replaced by Dvl2 inhibition. Importantly, they also show that PAPC has a function beyond PCP inhibition. This was also evident in reaggregation experiments. Dvl2-MO–injected BCR cells attached to uninjected cells to form close contacts, and the coexpression of PAPC was required to induce cleft contact formation (Fig. 7, E and F). The function of PAPC in this process does not depend on Snail1.


PAPC mediates self/non-self-distinction during Snail1-dependent tissue separation.

Luu O, Damm EW, Parent SE, Barua D, Smith TH, Wen JW, Lepage SE, Nagel M, Ibrahim-Gawel H, Huang Y, Bruce AE, Winklbauer R - J. Cell Biol. (2015)

PAPC function beyond PCP inhibition is required for cleft formation. (A) Quantitation of separation in gain-of-function experiment. BCR was injected as indicated. (B–D) Ectopic cleft formation in the BCR, as in Fig. 3 (G–L). (E) Exemplary kymographs of cleft contact formation, as in Fig. 4 E. (F) Frequency of cleft contacts after reaggregation, as in Fig. 4 C. (G) Reduced Dvl-GFP puncta in EphB4-MO–injected mesoderm (green) at boundary to BCR (red, membrane-RFP in ectoderm). (H) Quantitation of separation behavior. (left) Mesoderm injected as indicated was tested on normal BCR. (right) BCR explants injected as indicated were tested on normal BCR. (I) Model of tissue separation at the mesoderm–ectoderm (BCR) boundary.
© Copyright Policy - openaccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4362454&req=5

fig7: PAPC function beyond PCP inhibition is required for cleft formation. (A) Quantitation of separation in gain-of-function experiment. BCR was injected as indicated. (B–D) Ectopic cleft formation in the BCR, as in Fig. 3 (G–L). (E) Exemplary kymographs of cleft contact formation, as in Fig. 4 E. (F) Frequency of cleft contacts after reaggregation, as in Fig. 4 C. (G) Reduced Dvl-GFP puncta in EphB4-MO–injected mesoderm (green) at boundary to BCR (red, membrane-RFP in ectoderm). (H) Quantitation of separation behavior. (left) Mesoderm injected as indicated was tested on normal BCR. (right) BCR explants injected as indicated were tested on normal BCR. (I) Model of tissue separation at the mesoderm–ectoderm (BCR) boundary.
Mentions: PCP inhibition is not sufficient for boundary formation. In gain-of-function experiments, coinjection of Dvl2-MO and PAPC, but not Dvl2-MO alone, induced separation (Fig. 7 A). Moreover, when Dvl2-MO was expressed in half of the BCR, no boundary formed, but a cleft appeared when PAPC was coexpressed; the boundary vanished when PAPC was simultaneously expressed in the other half of the BCR (Fig. 7, B–D). These results confirm that Xsnail1 can be functionally replaced by Dvl2 inhibition. Importantly, they also show that PAPC has a function beyond PCP inhibition. This was also evident in reaggregation experiments. Dvl2-MO–injected BCR cells attached to uninjected cells to form close contacts, and the coexpression of PAPC was required to induce cleft contact formation (Fig. 7, E and F). The function of PAPC in this process does not depend on Snail1.

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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada M5S 3G5.

Show MeSH
Related in: MedlinePlus