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A feedback mechanism converts individual cell features into a supracellular ECM structure in Drosophila trachea.

Öztürk-Çolak A, Moussian B, Araújo SJ, Casanova J - Elife (2016)

Bottom Line: Furthermore, we reveal that cell-cell junctions are key players in this aECM patterning and organisation and that individual cells contribute autonomously to their aECM.Strikingly, changes in the aECM influence the levels of phosphorylated Src42A (pSrc) at cell junctions.Therefore, we propose that Src42A phosphorylation levels provide a link for the ECM environment to ensure proper cytoskeletal organisation.

View Article: PubMed Central - PubMed

Affiliation: Institut de Biologia Molecular de Barcelona, Parc Cientific de Barcelona, Barcelona, Spain.

ABSTRACT
The extracellular matrix (ECM), a structure contributed to and commonly shared by many cells in an organism, plays an active role during morphogenesis. Here, we used the Drosophila tracheal system to study the complex relationship between the ECM and epithelial cells during development. We show that there is an active feedback mechanism between the apical ECM (aECM) and the apical F-actin in tracheal cells. Furthermore, we reveal that cell-cell junctions are key players in this aECM patterning and organisation and that individual cells contribute autonomously to their aECM. Strikingly, changes in the aECM influence the levels of phosphorylated Src42A (pSrc) at cell junctions. Therefore, we propose that Src42A phosphorylation levels provide a link for the ECM environment to ensure proper cytoskeletal organisation.

No MeSH data available.


Related in: MedlinePlus

Apical cell shape in the Blimp-1 and kkv mutant embryos.Wild-type (A), Blimp-1 mutant (B) and kkv mutant (C) embryos stained with anti-DE-cad (red) to label the cell surface and fluostain (green) to label taenidial folds. In the Blimp-1 mutant embryo, apical cell shape is elongated perpendicular to the tube axis (B), whereas it is mostly parallel to the tube axis in the wild-type embryo (A). In the kkv mutant embryo, apical cell shape resembles more the Blimp-1 phenotype (C). The distinct apical cell shape of the fusion cells (A, arrow) does not seem to be affected by the loss of function of Blimp-1 (B, arrow) but is affected by the absence of kkv (C, arrow). The images are projections of confocal sections. Scale bars = 10 μm. (D-F) Wild-type (D) and Src42A mutant (E) embryos and the effect of constitutively activated Src42A on tracheal cells (F) of embryos stained with fluostain to label taenidial folds. The taenidial folds run perpendicular to the tube axis in wild-type (D), Src42A mutant (E) and Src42A;Src64B double mutant (G) embryos, whereas they are not properly formed in overexpression of Src42ACA embryos (F). The images are projections of confocal sections. Scale bars =10 μm.DOI:http://dx.doi.org/10.7554/eLife.09373.015
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fig7: Apical cell shape in the Blimp-1 and kkv mutant embryos.Wild-type (A), Blimp-1 mutant (B) and kkv mutant (C) embryos stained with anti-DE-cad (red) to label the cell surface and fluostain (green) to label taenidial folds. In the Blimp-1 mutant embryo, apical cell shape is elongated perpendicular to the tube axis (B), whereas it is mostly parallel to the tube axis in the wild-type embryo (A). In the kkv mutant embryo, apical cell shape resembles more the Blimp-1 phenotype (C). The distinct apical cell shape of the fusion cells (A, arrow) does not seem to be affected by the loss of function of Blimp-1 (B, arrow) but is affected by the absence of kkv (C, arrow). The images are projections of confocal sections. Scale bars = 10 μm. (D-F) Wild-type (D) and Src42A mutant (E) embryos and the effect of constitutively activated Src42A on tracheal cells (F) of embryos stained with fluostain to label taenidial folds. The taenidial folds run perpendicular to the tube axis in wild-type (D), Src42A mutant (E) and Src42A;Src64B double mutant (G) embryos, whereas they are not properly formed in overexpression of Src42ACA embryos (F). The images are projections of confocal sections. Scale bars =10 μm.DOI:http://dx.doi.org/10.7554/eLife.09373.015

Mentions: How could the apical chitin in the ECM influence actin bundling? We observed that both kkv and Blimp-1 mutations had an effect on tracheal cell shape. In the wild-type trachea, the cells of the DT were organised such that the longest axis of their apical shape is parallel to the tube axis. However, in both Blimp-1 and kkv mutant trachea (Figure 7B, C), the anteroposterior elongation of the cells of the DT was lost, causing cells to be more square shaped. Thus, we hypothesised that the change in taenidial orientation in kkv and Blimp-1 mutants could be attributed to the alteration in the overall orientation or shape of the tracheal cells. Interestingly, a modification of cell shape/orientation also occurs in embryos mutant for the Src-family kinase Src42A (Förster and Luschnig, 2012). However, and as previously reported for F-actin (Förster and Luschnig, 2012), we found taenidia to follow the same organisation in Src42A mutant embryos as the wild-type (Figure 7E) indicating that proper organisation of taenidia can be uncoupled from correct tracheal cell shape/orientation and thus that the former is not merely a consequence of the latter.10.7554/eLife.09373.015Figure 7.Apical cell shape in the Blimp-1 and kkv mutant embryos.


A feedback mechanism converts individual cell features into a supracellular ECM structure in Drosophila trachea.

Öztürk-Çolak A, Moussian B, Araújo SJ, Casanova J - Elife (2016)

Apical cell shape in the Blimp-1 and kkv mutant embryos.Wild-type (A), Blimp-1 mutant (B) and kkv mutant (C) embryos stained with anti-DE-cad (red) to label the cell surface and fluostain (green) to label taenidial folds. In the Blimp-1 mutant embryo, apical cell shape is elongated perpendicular to the tube axis (B), whereas it is mostly parallel to the tube axis in the wild-type embryo (A). In the kkv mutant embryo, apical cell shape resembles more the Blimp-1 phenotype (C). The distinct apical cell shape of the fusion cells (A, arrow) does not seem to be affected by the loss of function of Blimp-1 (B, arrow) but is affected by the absence of kkv (C, arrow). The images are projections of confocal sections. Scale bars = 10 μm. (D-F) Wild-type (D) and Src42A mutant (E) embryos and the effect of constitutively activated Src42A on tracheal cells (F) of embryos stained with fluostain to label taenidial folds. The taenidial folds run perpendicular to the tube axis in wild-type (D), Src42A mutant (E) and Src42A;Src64B double mutant (G) embryos, whereas they are not properly formed in overexpression of Src42ACA embryos (F). The images are projections of confocal sections. Scale bars =10 μm.DOI:http://dx.doi.org/10.7554/eLife.09373.015
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fig7: Apical cell shape in the Blimp-1 and kkv mutant embryos.Wild-type (A), Blimp-1 mutant (B) and kkv mutant (C) embryos stained with anti-DE-cad (red) to label the cell surface and fluostain (green) to label taenidial folds. In the Blimp-1 mutant embryo, apical cell shape is elongated perpendicular to the tube axis (B), whereas it is mostly parallel to the tube axis in the wild-type embryo (A). In the kkv mutant embryo, apical cell shape resembles more the Blimp-1 phenotype (C). The distinct apical cell shape of the fusion cells (A, arrow) does not seem to be affected by the loss of function of Blimp-1 (B, arrow) but is affected by the absence of kkv (C, arrow). The images are projections of confocal sections. Scale bars = 10 μm. (D-F) Wild-type (D) and Src42A mutant (E) embryos and the effect of constitutively activated Src42A on tracheal cells (F) of embryos stained with fluostain to label taenidial folds. The taenidial folds run perpendicular to the tube axis in wild-type (D), Src42A mutant (E) and Src42A;Src64B double mutant (G) embryos, whereas they are not properly formed in overexpression of Src42ACA embryos (F). The images are projections of confocal sections. Scale bars =10 μm.DOI:http://dx.doi.org/10.7554/eLife.09373.015
Mentions: How could the apical chitin in the ECM influence actin bundling? We observed that both kkv and Blimp-1 mutations had an effect on tracheal cell shape. In the wild-type trachea, the cells of the DT were organised such that the longest axis of their apical shape is parallel to the tube axis. However, in both Blimp-1 and kkv mutant trachea (Figure 7B, C), the anteroposterior elongation of the cells of the DT was lost, causing cells to be more square shaped. Thus, we hypothesised that the change in taenidial orientation in kkv and Blimp-1 mutants could be attributed to the alteration in the overall orientation or shape of the tracheal cells. Interestingly, a modification of cell shape/orientation also occurs in embryos mutant for the Src-family kinase Src42A (Förster and Luschnig, 2012). However, and as previously reported for F-actin (Förster and Luschnig, 2012), we found taenidia to follow the same organisation in Src42A mutant embryos as the wild-type (Figure 7E) indicating that proper organisation of taenidia can be uncoupled from correct tracheal cell shape/orientation and thus that the former is not merely a consequence of the latter.10.7554/eLife.09373.015Figure 7.Apical cell shape in the Blimp-1 and kkv mutant embryos.

Bottom Line: Furthermore, we reveal that cell-cell junctions are key players in this aECM patterning and organisation and that individual cells contribute autonomously to their aECM.Strikingly, changes in the aECM influence the levels of phosphorylated Src42A (pSrc) at cell junctions.Therefore, we propose that Src42A phosphorylation levels provide a link for the ECM environment to ensure proper cytoskeletal organisation.

View Article: PubMed Central - PubMed

Affiliation: Institut de Biologia Molecular de Barcelona, Parc Cientific de Barcelona, Barcelona, Spain.

ABSTRACT
The extracellular matrix (ECM), a structure contributed to and commonly shared by many cells in an organism, plays an active role during morphogenesis. Here, we used the Drosophila tracheal system to study the complex relationship between the ECM and epithelial cells during development. We show that there is an active feedback mechanism between the apical ECM (aECM) and the apical F-actin in tracheal cells. Furthermore, we reveal that cell-cell junctions are key players in this aECM patterning and organisation and that individual cells contribute autonomously to their aECM. Strikingly, changes in the aECM influence the levels of phosphorylated Src42A (pSrc) at cell junctions. Therefore, we propose that Src42A phosphorylation levels provide a link for the ECM environment to ensure proper cytoskeletal organisation.

No MeSH data available.


Related in: MedlinePlus