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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

Time course of actin ring and taenidial fold formation.(A–F) Projections of confocal sections of wild-type DTs from early stage 16 to stage 17. F-actin is detected by phalloidin (red) and Chitin by fluostain (blue). The F-actin (red) and chitin (blue) structures are schematically represented under each image. First F-actin bundles are formed at the fusion points during the fusion process of the DT (A’, arrows). These bundles are formed as a result of highly orchestrated cell shape changes during fusion events. At mid-stage 16, F-actin rings become visible along the DT while the taenidial folds are not fully formed yet and hence not labelled with fluostain (B). Then, very thin taenidial folds become visible (C). At first, they are not formed at fusion points (D). Later, taenidial folds at fusion points are also formed, thus generating a continuous taenidial structure along the tube (E). Finally, the taenidial folds and F-actin bundles reach their most mature form as the trachea start to fill with air (F). Both stainings are shown in the merge images (A-F). The fluostain (A’-F’) and phalloidin (A’’-F’’) stainings are shown separately.DOI:http://dx.doi.org/10.7554/eLife.09373.004
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fig1s1: Time course of actin ring and taenidial fold formation.(A–F) Projections of confocal sections of wild-type DTs from early stage 16 to stage 17. F-actin is detected by phalloidin (red) and Chitin by fluostain (blue). The F-actin (red) and chitin (blue) structures are schematically represented under each image. First F-actin bundles are formed at the fusion points during the fusion process of the DT (A’, arrows). These bundles are formed as a result of highly orchestrated cell shape changes during fusion events. At mid-stage 16, F-actin rings become visible along the DT while the taenidial folds are not fully formed yet and hence not labelled with fluostain (B). Then, very thin taenidial folds become visible (C). At first, they are not formed at fusion points (D). Later, taenidial folds at fusion points are also formed, thus generating a continuous taenidial structure along the tube (E). Finally, the taenidial folds and F-actin bundles reach their most mature form as the trachea start to fill with air (F). Both stainings are shown in the merge images (A-F). The fluostain (A’-F’) and phalloidin (A’’-F’’) stainings are shown separately.DOI:http://dx.doi.org/10.7554/eLife.09373.004

Mentions: Given the close correlation between taenidia and the rings of actin bundles (Matusek et al., 2006), we next analysed the developmental time course of these two structures in the same embryo. For this purpose, we used fluostain and phalloidin to visualise chitin and F-actin, respectively (Moussian et al., 2005; Araújo et al., 2005). At early stage 16, when taenidia were not yet detectable, we distinguished some actin rings in the cells of the DT (Figure 1G). It is noteworthy that the first actin rings to appear in the trachea were those corresponding to the fusion cells, which are not related to taenidia but instead to the fusion between the lumen of adjacent segments of the DT (Lee and Kolodziej, 2002). Shortly after, actin rings in other cells were detected throughout the length of the DT, but these were much weaker than those present in the fusion cells (Figure 1G’’). At this stage, remnants of the chitin filament were still detectable but taenidial folds were not (Figure 1G’). As the chitin filament faded away and taenidia became more visible, the actin rings became more defined and prominent (Figure 1H; for a more detailed time course of actin ring and taenidial fold formation see Figure 1—figure supplement 1).


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)

Time course of actin ring and taenidial fold formation.(A–F) Projections of confocal sections of wild-type DTs from early stage 16 to stage 17. F-actin is detected by phalloidin (red) and Chitin by fluostain (blue). The F-actin (red) and chitin (blue) structures are schematically represented under each image. First F-actin bundles are formed at the fusion points during the fusion process of the DT (A’, arrows). These bundles are formed as a result of highly orchestrated cell shape changes during fusion events. At mid-stage 16, F-actin rings become visible along the DT while the taenidial folds are not fully formed yet and hence not labelled with fluostain (B). Then, very thin taenidial folds become visible (C). At first, they are not formed at fusion points (D). Later, taenidial folds at fusion points are also formed, thus generating a continuous taenidial structure along the tube (E). Finally, the taenidial folds and F-actin bundles reach their most mature form as the trachea start to fill with air (F). Both stainings are shown in the merge images (A-F). The fluostain (A’-F’) and phalloidin (A’’-F’’) stainings are shown separately.DOI:http://dx.doi.org/10.7554/eLife.09373.004
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4764556&req=5

fig1s1: Time course of actin ring and taenidial fold formation.(A–F) Projections of confocal sections of wild-type DTs from early stage 16 to stage 17. F-actin is detected by phalloidin (red) and Chitin by fluostain (blue). The F-actin (red) and chitin (blue) structures are schematically represented under each image. First F-actin bundles are formed at the fusion points during the fusion process of the DT (A’, arrows). These bundles are formed as a result of highly orchestrated cell shape changes during fusion events. At mid-stage 16, F-actin rings become visible along the DT while the taenidial folds are not fully formed yet and hence not labelled with fluostain (B). Then, very thin taenidial folds become visible (C). At first, they are not formed at fusion points (D). Later, taenidial folds at fusion points are also formed, thus generating a continuous taenidial structure along the tube (E). Finally, the taenidial folds and F-actin bundles reach their most mature form as the trachea start to fill with air (F). Both stainings are shown in the merge images (A-F). The fluostain (A’-F’) and phalloidin (A’’-F’’) stainings are shown separately.DOI:http://dx.doi.org/10.7554/eLife.09373.004
Mentions: Given the close correlation between taenidia and the rings of actin bundles (Matusek et al., 2006), we next analysed the developmental time course of these two structures in the same embryo. For this purpose, we used fluostain and phalloidin to visualise chitin and F-actin, respectively (Moussian et al., 2005; Araújo et al., 2005). At early stage 16, when taenidia were not yet detectable, we distinguished some actin rings in the cells of the DT (Figure 1G). It is noteworthy that the first actin rings to appear in the trachea were those corresponding to the fusion cells, which are not related to taenidia but instead to the fusion between the lumen of adjacent segments of the DT (Lee and Kolodziej, 2002). Shortly after, actin rings in other cells were detected throughout the length of the DT, but these were much weaker than those present in the fusion cells (Figure 1G’’). At this stage, remnants of the chitin filament were still detectable but taenidial folds were not (Figure 1G’). As the chitin filament faded away and taenidia became more visible, the actin rings became more defined and prominent (Figure 1H; for a more detailed time course of actin ring and taenidial fold formation see Figure 1—figure supplement 1).

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