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Transient junction anisotropies orient annular cell polarization in the Drosophila airway tubes

Nature Cell Biology volume 17, pages 1569–1576 (2015)Cite this article

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Abstract

In contrast to planes, three-dimensional (3D) structures such as tubes are physically anisotropic. Tubular organs exhibit a striking orientation of landmarks according to the physical anisotropy of the 3D shape1,2,3,4, in addition to planar cell polarization5,6. However, the influence of 3D tissue topography on the constituting cells remains underexplored7,8,9. Here, we identify a regulatory network polarizing cellular biochemistry according to the physical anisotropy of the 3D tube geometry (tube cell polarization) by a genome-wide, tissue-specific RNAi screen. During Drosophila airway remodelling, each apical cellular junction is equipotent to establish perpendicular actomyosin cables, irrespective of the longitudinal or transverse tube axis. A dynamic transverse enrichment of atypical protein kinase C (aPKC) shifts the balance and transiently targets activated small GTPase RhoA, myosin phosphorylation and Rab11 vesicle trafficking to longitudinal junctions. We propose that the PAR complex translates tube physical anisotropy into longitudinal junctional anisotropy, where cell–cell communication aligns the contractile cytoskeleton of neighbouring cells.

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Figure 1: A genome-wide RNAi screen for regulators of airway morphogenesis and function in Drosophila.
Figure 2: MLC-dependent junctional Rab11 anisotropy during dynamic remodelling of the airway tubes.
Figure 3: A protein interaction network based on the 8 TCP genes identifies RhoA as a regulator of TCP orientation.
Figure 4: Transverse localization of the PAR complex orients the anisotropic RhoA activity.
Figure 5: Cell communication across longitudinal junctions aligns annular-TCP landmarks among neighbouring cells.

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Acknowledgements

We thank the members of the fly community, who isolated, characterized or distributed fly strains or antibodies, especially B. Dickson, K. Keleman, R. Klug, T. Micheler and the VDRC team for primary screen support, S. Bogdan, C. Doe, J. Knoblich, G. Longmore, J. Mihály, BDSC, NIG, TRiP and DSHB for strains and antibodies. We thank Flybase for the Drosophila genomic resources and M. Yamazaki for advice on the virginizer strain and database construction. We thank IFSU and members of the Mannervik, Samakovlis and Åström laboratories for support, especially M. Björk for fly service and V. Tsarouhas for continuous support. Thanks to C. Betsholtz, L. Claesson-Welsh, M. Mannervik, V. Tsarouhas and S. Åström for comments on the manuscript. We apologize for many reference omissions due to space limitation. This work was supported by grants from the Swedish Research Council and the Swedish Cancer Society to C.S. B.A. is a Royal Society University Research Fellow.

Author information

Author notes

  1. Chie Hosono and Ryo Matsuda: These authors contributed equally to this work.

Authors and Affiliations

  1. Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, S-10691 Stockholm, Sweden

    Chie Hosono, Ryo Matsuda & Christos Samakovlis

  2. Cambridge Systems Biology Centre, University of Cambridge, Cambridge CB2 1QR, UK

    Boris Adryan

  3. ECCPS, University of Giessen, Aulweg 130 35392 Giessen, Germany,

    Christos Samakovlis

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  1. Chie Hosono
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  2. Ryo Matsuda
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  4. Christos Samakovlis
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Contributions

C.H., R.M. and C.S. conceived, designed and supervised the project. C.S. directed the project to annular-TCP genes. C.H. and R.M. performed the primary screen. C.H. performed all other experiments. C.H. and R.M. initiated and B.A. extended and finalized the bioinformatics work. C.H., R.M., B.A. and C.S. analysed the bioinformatics data. C.H., R.M. and C.S. analysed the biological data. R.M. wrote the manuscript. C.H., R.M. and C.S. wrote the paper. B.A. finalized the bioinformatics part and commented on the rest.

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Correspondence to Christos Samakovlis.

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Integrated supplementary information

Supplementary Figure 1 A group of genes required for formation or orientation of annular F-actin bundles and aECM ridges: RNAi phenotypes and their validation by standard mutations.

a–h, Confocal projection of phalloidin staining showing the airway F-actin bundles of mid 2nd instar larvae (65 h AEL) (left) and light microscope view of the ECM morphology of third instar larvae (around 74 h AEL) (right). Compared to the DT of the control (a), E-cadherin (DE-cad)-RNAi (b), aPKC-RNAi (c), par6-RNAi (d) cause disorientation of annular-TCP landmarks while cdc42-RNAi (e), profilin (chic)-RNAi (f), DAAM-RNAi (g) and Act5C-RNAi (h) cause defective F-actin polymerization and short or irregular ECM ridges. Arrows in b indicate gaps between neighbouring cells. (i), Confocal projections of DT cells of mid 2nd instar larvae. rab11-RNAi expressing cells are marked with CD8-GFP (green or yellow dots). F-actin bundles are not formed in rab11-RNAi expressing cells and the bundles of adjacent wild-type cells are misaligned (arrow). j,k, Confocal views of the DT at 65 h AEL mid 2nd instar of the control (j) or aPKC-RNAi (k). Left, single sections of transmitted light image. Right, projection views of phalloidin staining. Arrowheads mark the apical lining of airway cells. Tube diameter expansion has occurred normally (left, arrowheads) till this stage while aPKC-RNAi causes disorientation of annular F-actin bundles compared to controls (right). l–t, Light microscope views of aECM ridges in early 2nd instar DT (at around 50 h AEL) (l–n) or early 3rd instar DT (at around 74 h AEL) (o–t). Compared to the control (l,o), mutants of cdc42 (m), DAAM (n) or aPKC (p) show disorientation of the aECM ridges. q–t, Clones marked with CD8-GFP (green, lower panels). Compared to the control (q), mutant clones of profilin (chic) (r), par6 (s) or E-cadherin (DE-cad) (t) show disruption or disorientation of the aECM ridges. Yellow dots mark clone borders. u–w, Light microscope views of the aECM ridges of early 3rd instar DT (at around 74 h AEL). The control (u), ft maternal and zygotic mutants (v) or ds zygotic mutant (w) have comparable regular aECM ridges. Scale bars: 20 μm. Fluorescent images in a–h are representative of at least 10 larvae from ≥ 5 independent experiments. Light microscope views in a–h are representative of at least 5 larvae from ≥ 2 independent experiments. Images in I are representative of at least 6 larvae from 2 independent experiments. Images in j and k are representative of at least 10 larva from ≥ 2 independent experiments. Images in l–p are representative of at least 4 larvae from 3 independent experiments. Images in q–t are representative of at least 5 larvae from ≥ 2 independent experiments. Images in u–w are representative of at least 6 larvae from ≥ 2 independent experiments.

Supplementary Figure 2 Dynamic localization of Rab11-GFP during airway remodelling.

a–d, Rab11-GFP staining at different time points during the second instar stage. Top: confocal projection views of DT. Middle: single sections of the lateral view for Rab11-GFP (middle) and bottom: transmitted light views. Yellow and black arrows mark the apical cell surface that becomes progressively separated from the old aECM lining. Rab11-GFP homogeneously distributes in the cytoplasm at 57 h AEL (a). Rab11-GFP accumulates apically by 62 h AEL, when lumen expansion had started (b) and shows a transient enrichment at longitudinal junctions (blue arrow) compared to transverse junctions (blue arrowhead) at 65 h AEL (c). The apical enrichment of Rab11-GFP is lost by 67 h AEL when tube expansion was completed (d). e, A schematic of the typical branches in a single metameric unit of the respiratory network. DT or transverse connectives (TC) branches are marked. f–h, Single confocal sections of the DT at 65 h AEL mid 2nd instar (f), or the TC, TC(I) (g) and TC(II) (h). From left to right, transmitted light image, Rab11-GFP staining (green), E-cadherin (DE-cad) staining (magenta) and merge of Rab11-GFP and E-cadherin (DE-cad). Rab11-GFP is enriched at the longitudinal junctions in all branches (arrow). Scale bars: 20 μm. Images in a–d are representative of at least 10 larvae from ≥ 2 independent experiments. Images in f are representative of at least 10 larvae from ≥ 2 independent experiments. Images in l–p are representative of at least 4 larvae from ≥ 3 independent experiments. Images in g and h are representative of at least 3 larvae from ≥ 2 independent experiments.

Supplementary Figure 3 Phenotypic validation of 2 candidate annular-TCP genes from the protein interaction network and anisotropic localization of key annular-TCP regulators during tube remodelling.

a–f, Validation of cip4 and PP1α-87B function in annular-TCP. Phalloidin staining of the DT at mid 2nd instar (65 h AEL) (a–c,f) or mid first instar (41 h AEL) (d,e). Compared to the controls (a,d), Cip4 overexpression (b) compromised F-actin bundle formation like RNAi of its interaction partner cdc42 (c) or DAAM (Supplementary Fig. 1g) while PP1α-87B-RNAi (e) caused disorientation of F-actin bundles like RNAi of its interaction partner par6 (f). g–l, Anisotropic localization of key annular- tube TCP regulators during remodelling. g, A summary showing the time course of localization of various TCP regulators at different stages of tube remodelling and expansion during 2nd instar larvae. Initiation of diametric tube expansion becomes evident when the old aECM lining detaches from the apical cell surface, which is followed by successive anisotropic localization of TCP regulators. T- and L- means transverse and longitudinal, respectively. Note that 2 molting cycles occur every 24 h at 25 °C. The different phases of tube remodelling and the anisotropic localization of TCP regulators occur at each molt. h–n, A confocal projection (h) or single sections (i–n) of the DT at 2nd instar larvae in the wild type. h, aPKC and Par6 show similar localization. Note that at this stage, in addition to their well-documented accumulation along the apical junctions, diffuse cytoplasmic localization occurs preferentially along the transverse junctions. i–l, At 63-64 h AEL, RhoGEF2 amount is low near the transverse junctions, where Par6-GFP accumulates (blue arrows in i,j) while RhoGEF2 becomes enriched at longitudinal junctions (yellow arrowheads in j). At 63.5–64.5 h AEL, longitudinal localization of RhoGEF2 (k) precedes Rab11-GFP enrichment (l) (arrowheads). m,n, RhoGEF2 signals (m) accumulate in the cytoplasm and are largely excluded from the apical regions marked with phalloidin (yellow arrows). In contrast, pMLC (n) predominantly localizes in apical regions (yellow arrows). Asterisks indicate lumens. Scale bars: 20 μm. Images in a–f are representative of at least 3 larvae from ≥ 2 independent experiments. Images in h are representative of at least 8 larvae from ≥ 4 independent experiments. Images in i-l are representative of at least 4 larvae from ≥ 2 independent experiments. Images in m and n are representative of at least 6 larvae from ≥ 3 independent experiments.

Supplementary Figure 4 Effects of manipulations of RhoA activity on TCP and rab11 interaction with RhoA signalling.

Confocal projections of the DT at 2nd instar larvae at 64–66 h AEL upon expression of a constitutive active form (a–c) or a dominant negative form (d–f) of RhoA. Flip-out clones using the Act5c>y>gal4 construct are marked by cytoplasmic GFP or CD8-GFP (green). DE-cad marks all junctions. RhoAV14 expression increases levels of pMLC (a) or phalloidin labelled F-actin cables (b) (arrows) while RhoAN19 expression decreases levels of pMLC (d) or phalloidin labelled F-actin cables (e) (arrows). In either situation, Rab11 is also mislocalised at the transverse junctions (c,f, arrows). We note that single cell clones of RhoAN19 do not change directions of annular-TCP (e compare with f), suggesting that neighbouring wild type cells can communicate the direction of annular-TCP. g, In rab11-RNAi expressing clones, preferential pMLC accumulation at longitudinal junctions is lost. Quantification is shown in h. (n = 29 for L and 20 for T junctions from 6 rab11-RNAi larva, NS, not significant by unpaired two-tailed Student’s t test). Error bar, s.e.m. See also Supplementary Table 3 for scatterplots. Scale bars: 20 μm. Images in a–c are representative of at least 4 larvae from ≥ 2 independent experiments. Images in d–f are representative of at least 3 larvae from 2 independent experiments. Data in g and h are aggregated from 3 independent experiments.

Supplementary Figure 5 Transverse aPKC localization upon knock down of chic, RhoA or Rab11. Uif involvement in annular-TCP.

Confocal projections of the DT of 2nd instar larvae (63 h AEL) showing the transverse aPKC localization (arrows) in the wild type (a), chic-RNAi (b), RhoAN19 (c) or rab11-RNAi. Flipped out clones of the Act5c>y>gal4 construct are marked with CD8-GFP (bottom) in c and d. e–g, Quantification of relative intensity of aPKC along longitudinal (L) or transverse junctions (T) in chic-RNAi (e), RhoAN19 (f) or rab11-RNAi (g) (n = 43 for L and 37 for T junctions from 6 chic-RNAi larvae, ∗∗∗∗P < 0.0001, n = 31 for L and 37 for T junctions from 6 RhoA N19 larvae, ∗∗∗∗P < 0.0001, n = 26 for L and 17 for T junctions from 4 rab11-RNAi larvae, ∗∗∗P = 0.0009 p-values were calculated using the unpaired two-tailed Students t-test). Error bar: s.e.m. Analysis of source data is also shown in Supplementary Table 3. h–i, Rab11-GFP localization of 2nd instar larvae (65 h AEL) in the control (h) or upon DE-cad-RNAi (i). j–k, Confocal projections of phalloidin staining of the DT at mid-1st instar (42 h AEL) (left) or light microscopic views of aECM ridges at early L2 (around 50 h AEL) (right). Compared to the control (j), uif-RNAi (k) causes aECM ridge disorientation, which is especially evident at cell junctions. l, A single confocal section of DT stained for Uif (green) and E-cadherin (DE-cad, magenta) at 64 h AEL. In addition to the broad apical staining, Uif is preferentially detected along the longitudinal junctions (arrowhead) compared to the transverse junctions (arrow). In addition to strong junctional signals, DE-cad antibody weakly stains the cytoplasm33. Scale bars: 20 μm. Images in a are representative of at least 10 larvae from ≥ 4 independent experiments. Data in b–g are aggregated from 2 independent experiments. Analysis of source data is also shown in Supplementary Table 3. Images in h and i are representative of at least 6 larvae from ≥ 2 independent experiments. Fluorescent images in j and k are representative of 6 larvae from ≥ 2 independent experiments. Light microscope views in j and k are representative of at least 10 larvae from ≥ 4 independent experiments. Images in l are representative of 6 larvae from 2 independent experiments.

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Hosono, C., Matsuda, R., Adryan, B. et al. Transient junction anisotropies orient annular cell polarization in the Drosophila airway tubes. Nat Cell Biol 17, 1569–1576 (2015). https://doi.org/10.1038/ncb3267

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