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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.

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

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Actin cortex at cleft contacts. (A–C) Ectoderm–ectoderm (A), mesoderm–mesoderm (B), and ectoderm–mesoderm (C) reaggregating cells filled with cascade blue–dextran (blue; ectoderm) or RDA (red; mesoderm) and stained with fluorescein-tagged phalloidin for F-actin cortex labeling. Arrowhead in C indicates a cleft contact. (C’) High-magnification view of part of cleft contact in C; small arrows indicate gap largely covered by phalloidin staining; large arrow indicates gap remaining between cortices of adjacent cells. (D) Z stack of cleft contact; F-actin staining (bottom) is peripheral to RDA (top and bottom) boundary (arrowheads) both above cleft (top arrowheads) and in cleft (bottom arrowheads). (E) GFP-LifeAct (green) in gap (arrowhead) between living mesoderm and ectoderm cells labeled as in A–D.
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fig10: Actin cortex at cleft contacts. (A–C) Ectoderm–ectoderm (A), mesoderm–mesoderm (B), and ectoderm–mesoderm (C) reaggregating cells filled with cascade blue–dextran (blue; ectoderm) or RDA (red; mesoderm) and stained with fluorescein-tagged phalloidin for F-actin cortex labeling. Arrowhead in C indicates a cleft contact. (C’) High-magnification view of part of cleft contact in C; small arrows indicate gap largely covered by phalloidin staining; large arrow indicates gap remaining between cortices of adjacent cells. (D) Z stack of cleft contact; F-actin staining (bottom) is peripheral to RDA (top and bottom) boundary (arrowheads) both above cleft (top arrowheads) and in cleft (bottom arrowheads). (E) GFP-LifeAct (green) in gap (arrowhead) between living mesoderm and ectoderm cells labeled as in A–D.

Mentions: Ultrastructural gaps between cell pairs were often narrow and perhaps inconsistent with the pronounced gaps observed by light microscopy. We therefore asked whether exclusion of fluorescent dextran from the cell periphery contributed to how wide gaps appeared. In reaggregated cell pairs, phalloidin staining revealed prominent F-actin cortices (Fig. 10, A–D). Between ectoderm–ectoderm or mesoderm–mesoderm pairs, no gaps were observed using dextran labeling, and F-actin staining at the interface was very weak (Fig. 10, A and B), consistent with a reduction in cortex density upon adhesion in these cells (David et al., 2014). At ectoderm–mesoderm contacts, F-actin staining overlapped considerably, though not completely, with the dextran-contrasted gaps between cells (Fig. 10, C and C′), in agreement with the presence of both large and narrow gaps at the ultrastructural level. F-actin staining was also peripheral to the dextran label at free cell surfaces above contacts (Fig. 10 D). Exclusion of dextran from the cortices of ectoderm–mesoderm pairs was also observed in living cells labeled with LifeAct (Fig. 10 E).


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)

Actin cortex at cleft contacts. (A–C) Ectoderm–ectoderm (A), mesoderm–mesoderm (B), and ectoderm–mesoderm (C) reaggregating cells filled with cascade blue–dextran (blue; ectoderm) or RDA (red; mesoderm) and stained with fluorescein-tagged phalloidin for F-actin cortex labeling. Arrowhead in C indicates a cleft contact. (C’) High-magnification view of part of cleft contact in C; small arrows indicate gap largely covered by phalloidin staining; large arrow indicates gap remaining between cortices of adjacent cells. (D) Z stack of cleft contact; F-actin staining (bottom) is peripheral to RDA (top and bottom) boundary (arrowheads) both above cleft (top arrowheads) and in cleft (bottom arrowheads). (E) GFP-LifeAct (green) in gap (arrowhead) between living mesoderm and ectoderm cells labeled as in A–D.
© Copyright Policy - openaccess
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4362454&req=5

fig10: Actin cortex at cleft contacts. (A–C) Ectoderm–ectoderm (A), mesoderm–mesoderm (B), and ectoderm–mesoderm (C) reaggregating cells filled with cascade blue–dextran (blue; ectoderm) or RDA (red; mesoderm) and stained with fluorescein-tagged phalloidin for F-actin cortex labeling. Arrowhead in C indicates a cleft contact. (C’) High-magnification view of part of cleft contact in C; small arrows indicate gap largely covered by phalloidin staining; large arrow indicates gap remaining between cortices of adjacent cells. (D) Z stack of cleft contact; F-actin staining (bottom) is peripheral to RDA (top and bottom) boundary (arrowheads) both above cleft (top arrowheads) and in cleft (bottom arrowheads). (E) GFP-LifeAct (green) in gap (arrowhead) between living mesoderm and ectoderm cells labeled as in A–D.
Mentions: Ultrastructural gaps between cell pairs were often narrow and perhaps inconsistent with the pronounced gaps observed by light microscopy. We therefore asked whether exclusion of fluorescent dextran from the cell periphery contributed to how wide gaps appeared. In reaggregated cell pairs, phalloidin staining revealed prominent F-actin cortices (Fig. 10, A–D). Between ectoderm–ectoderm or mesoderm–mesoderm pairs, no gaps were observed using dextran labeling, and F-actin staining at the interface was very weak (Fig. 10, A and B), consistent with a reduction in cortex density upon adhesion in these cells (David et al., 2014). At ectoderm–mesoderm contacts, F-actin staining overlapped considerably, though not completely, with the dextran-contrasted gaps between cells (Fig. 10, C and C′), in agreement with the presence of both large and narrow gaps at the ultrastructural level. F-actin staining was also peripheral to the dextran label at free cell surfaces above contacts (Fig. 10 D). Exclusion of dextran from the cortices of ectoderm–mesoderm pairs was also observed in living cells labeled with LifeAct (Fig. 10 E).

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