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Cortical forces and CDC-42 control clustering of PAR proteins for Caenorhabditis elegans embryonic polarization

Abstract

Cell polarization enables zygotes to acquire spatial asymmetry, which in turn patterns cellular and tissue axes during development. Local modification in the actomyosin cytoskeleton mediates spatial segregation of partitioning-defective (PAR) proteins at the cortex1,2,3, but how mechanical changes in the cytoskeleton are transmitted to PAR proteins remains elusive. Here we uncover a role of actomyosin contractility in the remodelling of PAR proteins through cortical clustering. During embryonic polarization in Caenorhabditis elegans, actomyosin contractility and the resultant cortical tension stimulate clustering of PAR-3 at the cortex. Clustering of atypical protein kinase C (aPKC) is supported by PAR-3 clusters and is antagonized by activation of CDC-42. Cortical clustering is associated with retardation of PAR protein exchange at the cortex and with effective entrainment of advective cortical flows. Our findings delineate how cytoskeleton contractility couples the cortical clustering and long-range displacement of PAR proteins during polarization. The principles described here would apply to other pattern formation processes that rely on local modification of cortical actomyosin and PAR proteins.

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Figure 1: Dynamic cortical clusters of aPARs.
Figure 2: Cortical tension by actomyosin contractility stimulates clustering of PAR-3.
Figure 3: Active CDC-42 restricts accumulation of PKC-3 to PAR-3 clusters.
Figure 4: Cortical clustering is associated with efficient translocation of cortical aPARs.

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References

  1. Hoege, C. & Hyman, A. A. Principles of PAR polarity in Caenorhabditis elegans embryos. Nat. Rev. Mol. Cell Biol. 14, 315–322 (2013).

    Article  CAS  Google Scholar 

  2. Kemphues, K. PARsing embryonic polarity. Cell 101, 345–348 (2000).

    Article  CAS  Google Scholar 

  3. Goldstein, B. & Macara, I. G. The PAR proteins: fundamental players in animal cell polarization. Dev. Cell 13, 609–622 (2007).

    Article  CAS  Google Scholar 

  4. Munro, E., Nance, J. & Priess, J. R. Cortical flows powered by asymmetrical contraction transport PAR proteins to establish and maintain anterior-posterior polarity in the early C. elegans embryo. Dev. Cell 7, 413–424 (2004).

    Article  CAS  Google Scholar 

  5. Goehring, N. W. et al. Polarization of PAR proteins by advective triggering of a pattern-forming system. Science 334, 1137–1141 (2011).

    Article  CAS  Google Scholar 

  6. Dawes, A. T. & Munro, E. M. PAR-3 oligomerization may provide an actin-independent mechanism to maintain distinct par protein domains in the early Caenorhabditis elegans embryo. Biophys. J. 101, 1412–1422 (2011).

    Article  CAS  Google Scholar 

  7. Blanchoud, S., Busso, C., Naef, F. & Gonczy, P. Quantitative analysis and modeling probe polarity establishment in C. elegans embryos. Biophys. J. 108, 799–809 (2015).

    Article  CAS  Google Scholar 

  8. Cheeks, R. J. et al. C. elegans PAR proteins function by mobilizing and stabilizing asymmetrically localized protein complexes. Curr. Biol. 14, 851–862 (2004).

    Article  CAS  Google Scholar 

  9. Etemad-Moghadam, B., Guo, S. & Kemphues, K. J. Asymmetrically distributed PAR-3 protein contributes to cell polarity and spindle alignment in early C. elegans embryos. Cell 83, 743–752 (1995).

    Article  CAS  Google Scholar 

  10. Hung, T. J. & Kemphues, K. J. PAR-6 is a conserved PDZ domain-containing protein that colocalizes with PAR-3 in Caenorhabditis elegans embryos. Development 126, 127–135 (1999).

    CAS  PubMed  Google Scholar 

  11. Tabuse, Y. et al. Atypical protein kinase C cooperates with PAR-3 to establish embryonic polarity in Caenorhabditis elegans. Development 125, 3607–3614 (1998).

    CAS  PubMed  Google Scholar 

  12. Kumfer, K. T. et al. CGEF-1 and CHIN-1 regulate CDC-42 activity during asymmetric division in the Caenorhabditis elegans embryo. Mol. Biol. Cell 21, 266–277 (2010).

    Article  CAS  Google Scholar 

  13. Sailer, A., Anneken, A., Li, Y., Lee, S. & Munro, E. Dynamic opposition of clustered proteins stabilizes cortical polarity in the C. elegans zygote. Dev. Cell 35, 131–142 (2015).

    Article  CAS  Google Scholar 

  14. Varnai, P. & Balla, T. Visualization of phosphoinositides that bind pleckstrin homology domains: calcium- and agonist-induced dynamic changes and relationship to myo-[3H]inositol-labeled phosphoinositide pools. J. Cell Biol. 143, 501–510 (1998).

    Article  CAS  Google Scholar 

  15. Mayer, M., Depken, M., Bois, J. S., Julicher, F. & Grill, S. W. Anisotropies in cortical tension reveal the physical basis of polarizing cortical flows. Nature 467, 617–621 (2010).

    Article  CAS  Google Scholar 

  16. Zonies, S., Motegi, F., Hao, Y. & Seydoux, G. Symmetry breaking and polarization of the C. elegans zygote by the polarity protein PAR-2. Development 137, 1669–1677 (2010).

    Article  CAS  Google Scholar 

  17. Davies, T. et al. High-resolution temporal analysis reveals a functional timeline for the molecular regulation of cytokinesis. Dev. Cell 30, 209–223 (2014).

    Article  CAS  Google Scholar 

  18. Liu, J., Maduzia, L. L., Shirayama, M. & Mello, C. C. NMY-2 maintains cellular asymmetry and cell boundaries, and promotes a SRC-dependent asymmetric cell division. Dev. Biol. 339, 366–373 (2010).

    Article  CAS  Google Scholar 

  19. Willis, J. H., Munro, E., Lyczak, R. & Bowerman, B. Conditional dominant mutations in the Caenorhabditis elegans gene act-2 identify cytoplasmic and muscle roles for a redundant actin isoform. Mol. Biol. Cell 17, 1051–1064 (2006).

    Article  CAS  Google Scholar 

  20. O’Rourke, S. M. et al. A survey of new temperature-sensitive, embryonic-lethal mutations in C. elegans: 24 alleles of thirteen genes. PLoS ONE 6, e16644 (2011).

    Article  Google Scholar 

  21. Houk, A. R. et al. Membrane tension maintains cell polarity by confining signals to the leading edge during neutrophil migration. Cell 148, 175–188 (2012).

    Article  CAS  Google Scholar 

  22. Raucher, D. & Sheetz, M. P. Cell spreading and lamellipodial extension rate is regulated by membrane tension. J. Cell Biol. 148, 127–136 (2000).

    Article  CAS  Google Scholar 

  23. Tsujita, K., Takenawa, T. & Itoh, T. Feedback regulation between plasma membrane tension and membrane-bending proteins organizes cell polarity during leading edge formation. Nat. Cell Biol. 17, 749–758 (2015).

    Article  CAS  Google Scholar 

  24. Boulant, S., Kural, C., Zeeh, J. C., Ubelmann, F. & Kirchhausen, T. Actin dynamics counteract membrane tension during clathrin-mediated endocytosis. Nat. Cell Biol. 13, 1124–1131 (2011).

    Article  CAS  Google Scholar 

  25. Ziman, M., O’Brien, J. M., Ouellette, L. A., Church, W. R. & Johnson, D. I. Mutational analysis of CDC42Sc, a Saccharomyces cerevisiae gene that encodes a putative GTP-binding protein involved in the control of cell polarity. Mol. Cell. Biol. 11, 3537–3544 (1991).

    Article  CAS  Google Scholar 

  26. Li, J. et al. Binding to PKC-3, but not to PAR-3 or to a conventional PDZ domain ligand, is required for PAR-6 function in C. elegans. Dev. Biol. 340, 88–98 (2010).

    Article  CAS  Google Scholar 

  27. Naganathan, S. R., Furthauer, S., Nishikawa, M., Julicher, F. & Grill, S. W. Active torque generation by the actomyosin cell cortex drives left-right symmetry breaking. eLife 3, e04165 (2014).

    Article  Google Scholar 

  28. Cuenca, A. A., Schetter, A., Aceto, D., Kemphues, K. & Seydoux, G. Polarization of the C. elegans zygote proceeds via distinct establishment and maintenance phases. Development 130, 1255–1265 (2003).

    Article  CAS  Google Scholar 

  29. Motegi, F. et al. Microtubules induce self-organization of polarized PAR domains in Caenorhabditis elegans zygotes. Nat. Cell Biol. 13, 1361–1367 (2011).

    Article  CAS  Google Scholar 

  30. Hoege, C. et al. LGL can partition the cortex of one-cell Caenorhabditis elegans embryos into two domains. Curr. Biol. 20, 1296–1303 (2010).

    Article  CAS  Google Scholar 

  31. Beatty, A., Morton, D. & Kemphues, K. The C. elegans homolog of Drosophila Lethal giant larvae functions redundantly with PAR-2 to maintain polarity in the early embryo. Development 137, 3995–4004 (2010).

    Article  CAS  Google Scholar 

  32. Beers, M. & Kemphues, K. Depletion of the co-chaperone CDC-37 reveals two modes of PAR-6 cortical association in C. elegans embryos. Development 133, 3745–3754 (2006).

    Article  CAS  Google Scholar 

  33. Robin, F. B., McFadden, W. M., Yao, B. & Munro, E. M. Single-molecule analysis of cell surface dynamics in Caenorhabditis elegans embryos. Nat. Methods 11, 677–682 (2014).

    Article  CAS  Google Scholar 

  34. Marston, D. J. et al. MRCK-1 drives apical constriction in C. elegans by linking developmental patterning to force generation. Curr. Biol. 26, 2079–2089 (2016).

    Article  CAS  Google Scholar 

  35. McKinley, R. F., Yu, C. G. & Harris, T. J. Assembly of Bazooka polarity landmarks through a multifaceted membrane-association mechanism. J. Cell Sci. 125, 1177–1190 (2012).

    Article  CAS  Google Scholar 

  36. Krahn, M. P., Klopfenstein, D. R., Fischer, N. & Wodarz, A. Membrane targeting of Bazooka/PAR-3 is mediated by direct binding to phosphoinositide lipids. Curr. Biol. 20, 636–642 (2010).

    Article  CAS  Google Scholar 

  37. Wu, H. et al. PDZ domains of Par-3 as potential phosphoinositide signaling integrators. Mol. Cell 28, 886–898 (2007).

    Article  CAS  Google Scholar 

  38. Horikoshi, Y., Hamada, S., Ohno, S. & Suetsugu, S. Phosphoinositide binding by par-3 involved in par-3 localization. Cell Struct. Funct. 36, 97–102 (2011).

    Article  CAS  Google Scholar 

  39. Hartman, N. C. & Groves, J. T. Signaling clusters in the cell membrane. Curr. Opin. Cell Biol. 23, 370–376 (2011).

    Article  CAS  Google Scholar 

  40. Verkhovsky, A. B., Svitkina, T. M. & Borisy, G. G. Self-polarization and directional motility of cytoplasm. Curr. Biol. 9, 11–20 (1999).

    Article  CAS  Google Scholar 

Download references

Acknowledgements

This study was supported by the Singapore National Research Foundation (NRF_NRFF2012-08 (F.M.)) and the Strategic Japan-Singapore Cooperative Research Program by the Japan Science and Technology Agency and the Singapore Agency for Science, Technology, and Research (1514324022 (F.M.)). We are grateful to B. Goldstein and D. Dickinson (The University of North Carolina at Chapel Hill), K. Kemphues (Cornell University), J. C. F. Li, F. Margadant, H. T. Ong and A. Bershadsky (Mechanobiology Institute, Singapore), G. Seydoux (Johns Hopkins University), S. Mathew (Temasek Life-sciences Laboratory, Singapore), and the Caenorhabditis Genetic Center for strains, reagents and expertise. We thank B. Goldstein, D. Dickinson and N. Goehring (The Francis Crick Institute) for sharing their results with us before publication. We also thank A. Wong (Mechanobiology Institute, Singapore) and members in the Motegi laboratory for helpful comments on the manuscript.

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Authors and Affiliations

Authors

Contributions

The experimental design and presented ideas were developed together by all authors. F.M. guided the study and wrote the manuscript with input from all authors. S.-C.W. performed experiments in Figs 1, 3 and 4a, b and Supplementary Figs 1, 3 and 4a. T.Y.F.L. performed experiments in Figs 2 and 4c–g and Supplementary Figs 2 and 4b. Y.N. performed experiments in Fig. 2i–k and Supplementary Fig. 2c, d. L.G. and W.Y. developed program codes for PIV analysis and cortical cluster quantification, and analysed videos shown in Fig. 4c–g and Supplementary Fig. 4b.

Corresponding authors

Correspondence to Weimiao Yu or Fumio Motegi.

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The authors declare no competing financial interests.

Integrated supplementary information

Supplementary Figure 1 Dynamic cortical clusters of aPARs.

(a) Schematic representation of a zygote undergoing embryonic polarization before symmetry breaking, during early (EE), middle (EM) and late (EL) establishment phases, and maintenance phase (MA), and nuclear envelope break down (NEBD) to cytokinesis. The EE to EM phases take place during mitotic prophase after symmetry breaking, when cortical actomyosin develops advected flows toward the anterior pole. The EL phase is the transition phase when cortical contraction ceases, leaving a deeper-furrow at the anteroposterior midline. The MA phase occurs during prometaphase. We used the onset of cytokinesis, which was visualized by the rotation of cortical NMY-2::Kate, PAR-3::GFP, PKC-3::GFP, and GFP::CDC-42, as a respective time point for all time-lapse movies. (b) Detection and classification of cortical clusters. Representative PAR-3::GFP images are shown of a raw image after background subtraction, a segmented binary image of cortical clusters, the local maxima within the segmented clusters defined by peak-detection algorithm, and classification of each peak based on goodness of fitting (R2) to the 2D Gaussian function. Peaks with an R2 value over and below 0.6 are shown in green and red, respectively. (c) Representative images of live zygotes expressing PAR-3::GFP and PKC-3::GFP taken by spinning-disc confocal microscopy (SDC) and total-internal-reflection-fluorescence microscopy (TIRF). All images are representative of 5 zygotes from 3 independent experiments. Scale bar, 5 μm. (d) Representative time-lapse images of a zygote expressing GFP::CDC-42 and mChery::PHPLC and a zygote expressing GFP::WSP-1CRIB. GFP::CDC-42, mCherry::PHPLC, and GFP::WSP-1CRIB appeared at the cortex as an anterior-enriched gradient and eventually formed cortical foci on the anterior cortex in the middle-to-late establishment phase (EML). The times stated are with respect to the onset of cytokinesis. Scale bar, 5 μm. (e) The graphs show relative fluorescence intensity of cortical GFP::CDC-42, mCherry::PHPLC, and GFP::WSP-1CRIB foci during the EE, EML, and MA phases. Mean ± s.d. from n = 5 zygotes from 3 independent experiments. Source data can be found in Supplementary Table 3. (f) The histograms show the distribution of intensity of PAR-3::GFP and PKC-3::GFP clusters during polarization in wild-type zygotes. Black and grey bars represent clusters with an R2 value from 2D Gaussian fitting over and below 0.6, respectively. Mean ± s.d. from n = 6 zygotes for EE phase and n = 7 zygotes each for other phases of polarization.

Supplementary Figure 2 Cortical tension by actomyosin contractility stimulates clustering of PAR-3.

(a) Representative images of live zygotes expressing PAR-3::GFP, PKC-3::GFP, and GFP::CDC-42 under control, par-6(RNAi), par-3(RNAi), and pkc-3(RNAi) conditions. All images are representative of at least 10 zygotes from 3 independent experiments. Scale bar, 5 μm. PAR-3::GFP formed cortical clusters in par-6(RNAi) and pkc-3(RNAi) zygotes, while PKC-3::GFP no longer appeared as clusters in par-3(RNAi) zygotes. Treatment with par-3(RNAi), pkc-3(RNAi), and par-6(RNAi) caused GFP::CDC-42 to appear throughout the cortex. (b) Time-lapse sequence of PAR-3::GFP cluster assembly in nmy-2(ne3409) zygotes treated with hypotonic buffer. The formation of 20 clusters was tracked from 2 zygotes, and the graphs show changes in intensity over time for 10 clusters. The times stated are with respect to the appearances of PAR-3::GFP cluster. PAR-3::GFP appeared as a small puncta at the cortex and progressively increased in intensity. (c) The histograms show the distribution of intensity of PAR-3::GFP and PKC-3::GFP clusters in nmy-2(ne3409) zygotes treated with or without hypotonic buffer and nmy-2(ne3409) zygotes depleted of CDC-42. Black and grey bars represent clusters with an R2 value from 2D Gaussian fitting over and below 0.6, respectively. Mean ± s.d. from n = 7 zygotes for control, n = 6 zygotes for PAR-3::GFP in nmy-2(ne3409) treated with hypotonic buffer, and n = 5 zygotes each for other conditions. (d) The histograms show the distribution of cortical cluster intensity of GFP-tagged PAR-3 in NIH3T3 cells treated with or without hypotonic buffer in the presence of Blebbistatin. Black and grey bars represent clusters with an R2 value from 2D Gaussian fitting over and below 0.6, respectively. Mean ± s.d. from n = 12 cells for control and n = 24 cells each for all other conditions. (e) Representative images of live NIH3T3 cells expressing GFP-tagged C. elegans PAR-3 with or without treatment with 1 μM Latrunculin-A, a drug that depolymerize filamentous actin. All images are representative of 5 cells at each condition from 3 independent experiments.

Supplementary Figure 3 Active CDC-42 restricts accumulation of PKC-3 to PAR-3 clusters.

(a) The histograms show the distribution of intensity of PAR-3::GFP and PKC-3::GFP clusters during the establishment phases in zygotes expressing CDC-42Q61L, cdc-42(RNAi) zygotes, and cgef-1(RNAi) zygotes. Black and grey bars represent clusters with an R2 value from 2D Gaussian fitting over and below 0.6, respectively. Mean ± s.d. from n = 7 zygotes for wild type (EM phase) and cdc-42(RNAi), n = 6 for wild type (EE phase), and n = 5 each for other conditions. (b) Representative images of live zygotes expressing GFP::CDC-42, GFP::WSP-1CRIB, and GFP::PHPLC in wild-type, pkc-3(RNAi), nmy-2(ne3409), and cdc-42(RNAi) zygotes. All images are representative of 10 zygotes from 3 independent experiments. Scale bar, 5 μm. Cortical foci of GFP::CDC-42, GFP::WSP-1CRIB, and GFP::PHPLC were observed in pkc-3(RNAi) and nmy-2(ne3409) zygotes, where cortical contractility was low or inhibited, respectively. Cortical foci of GFP::PHPLC were observed in cdc-42(RNAi) zygotes.

Supplementary Figure 4 Cortical clustering is associated with efficient translocation of aPARs at the cortex.

(a) Fluorescence recovery after photo-bleaching (FRAP) analysis of PAR-3::GFP and PKC-3::GFP at the cortex during polarization. FRAP was performed on the anteromedial cortex of wild-type zygotes. Mean ± s.d. from at least 5 zygotes at each stage of polarization from 5 independent experiments. (b) Representative time-lapse images of live zygotes expressing NMY-2::Kate and PAR-3::GFP. Particle Image Velocimetry (PIV) analysis shows the orientation and magnitude of displacement of PAR-3::GFP and NMY-2::Kate in the PIV map (red arrows show NMY-2::Kate and blue arrows indicate PAR-3::GFP). The magnitude of PIV vectors is shown as a heat-map scale ranging from blue (lower value) to red (higher value). The cross-correlation of the orientation of PAR-3::GFP and NMY-2::Kate vectors depicts the magnitude of advective co-migratory behavior as a heat-map scale from blue (from 0 to −1) to red (+1). The times stated are with respect to the onset of symmetry breaking. Scale bar, 5 μm.

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Supplementary Information (PDF 68 kb)

Supplementary Table 1

Supplementary Information (XLSX 25 kb)

Supplementary Table 2

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Supplementary Table 3

Supplementary Information (XLSX 73 kb)

Cortical PAR-3::GFP with mCherry::PAR-6 in a one-cell stage wild-type zygote.

Scale bar, 5 μm. Related to Fig. 1a, c, d, g and Supplementary Fig. 1b, c, f. (MOV 2598 kb)

Cortical PKC-3::GFP with mCherry::PAR-6 in a one-cell stage wild-type zygote.

Scale bar, 5 μm. Related to Fig. 1a, e, f, g and Supplementary Fig. 1c, f. (MOV 2840 kb)

Cortical GFP::CDC-42 with mCherry::PAR-6 in a one-cell stage wild-type zygote.

Scale bar, 5 μm. Related to Fig. 1a, g. (MOV 5677 kb)

Cortical PAR-3::GFP, PKC-3::GFP and GFP::CDC-42 with mCherry::PHPLC in one-cell stage wild-type zygotes.

Images show the anteromedial cortex and are aligned to disassembly of cortical clusters and cortical foci. Scale bar, 5 μm. Related to Fig. 1b, g.i and Supplementary Fig. 1d, e. (MOV 1906 kb)

Cortical PKC-3::GFP and NMY-2::Kate during cytokinesis phase in a plk-1(or683) zygote.

Images show the medial cortex. Scale bar, 5 μm. Related to Fig. 2b, c. (MOV 661 kb)

Cortical PAR-3::GFP in nmy-2(ne3409) zygotes treated with or without hypotonic buffer.

Images show the anteromedial cortex. Scale bar, 5 μm. Related to Fig. 2d, e, f and Supplementary Fig. 2b, c. (MOV 378 kb)

Cortical PAR-3::GFP during establishment phases in control and mCherry::CDC-42Q61L expressing zygotes.

Images show the anteromedial cortex and are aligned to disassembly of cortical clusters. Scale bar, 5 μm. Related to Fig. 3b, c and Supplementary Fig. 3a. (MOV 235 kb)

Cortical PKC-3::GFP during establishment phases in control and mCherry::CDC-42Q61L expressing zygotes.

Images show the anteromedial cortex and are aligned to disassembly of cortical clusters. Scale bar, 5 μm. Related to Fig. 3b, d and Supplementary Fig. 3a. (MOV 236 kb)

Cortical PAR-3::GFP during establishment phases in control, cdc-42(RNAi), and cgef-1(RNAi) zygotes.

Images show the anteromedial cortex and are aligned to disassembly of cortical clusters. Scale bar, 5 μm. Related to Fig. 3b, e and Supplementary Fig. 3a. (MOV 792 kb)

Cortical PKC-3::GFP during establishment phases in control, cdc-42(RNAi), and cgef-1(RNAi) zygotes.

Images show the anteromedial cortex and are aligned to disassembly of cortical clusters. Scale bar, 5 μm. Related to Fig. 3b, f and Supplementary Fig. 3a. (MOV 661 kb)

Cortical PAR-3::GFP and mCherry::PHPLC during establishment phases in control and cdc-42(RNAi) zygotes.

Images show the anteromedial cortex and are aligned to disassembly of cortical clusters. Inverted PAR-3::GFP images are shown above in parallel. Scale bar, 5 μm. Related to Fig. 1i and Fig. 3g. (MOV 1382 kb)

Cortical PKC-3::GFP and mCherry::PHPLC during establishment phases in control and cdc-42(RNAi) zygotes.

Images show the anteromedial cortex and are aligned to disassembly of cortical clusters. Inverted PKC-3::GFP images are shown above in parallel. Scale bar, 5 μm. Related to Fig. 1i and Fig. 3i. (MOV 1197 kb)

Representative FRAP images of PAR-3::GFP and PKC-3::GFP during the early establishment phase in wild-type zygotes.

Images show the anteromedial cortex, where a 5 μm diameter circular area was photo-bleached, and are aligned to the onset of photo-bleaching. Scale bar, 5 μm. Related to Fig. 4a, b and Supplementary Fig. 4a. (MOV 3415 kb)

PIV analysis of cortical PAR-3::GFP and NMY-2::Kate during establishment phases in wild-type zygote.

Cortical PAR-3::GFP and NMY-2::Kate, segmented clusters of PAR-3::GFP, PIV vector maps, PIV magnitudes for PAR-3::GFP and NMY-2::Kate, as well as cross-correlation of two PIV vectors orientations are shown synchronically. Scale bar, 5 μm. Related to Fig. 4c–g and Supplementary Fig. 4b. (MOV 28337 kb)

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Wang, SC., Low, T., Nishimura, Y. et al. Cortical forces and CDC-42 control clustering of PAR proteins for Caenorhabditis elegans embryonic polarization. Nat Cell Biol 19, 988–995 (2017). https://doi.org/10.1038/ncb3577

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