Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Article
  • Published:

YAP and TAZ control peripheral myelination and the expression of laminin receptors in Schwann cells

Nature Neuroscience volume 19, pages 879–887 (2016)Cite this article

Subjects

Abstract

Myelination is essential for nervous system function. Schwann cells interact with neurons and the basal lamina to myelinate axons using known receptors, signals and transcription factors. In contrast, the transcriptional control of axonal sorting and the role of mechanotransduction in myelination are largely unknown. Yap and Taz are effectors of the Hippo pathway that integrate chemical and mechanical signals in cells. We describe a previously unknown role for the Hippo pathway in myelination. Using conditional mutagenesis in mice, we show that Taz is required in Schwann cells for radial sorting and myelination and that Yap is redundant with Taz. Yap and Taz are activated in Schwann cells by mechanical stimuli and regulate Schwann cell proliferation and transcription of basal lamina receptor genes, both necessary for radial sorting of axons and subsequent myelination. These data link transcriptional effectors of the Hippo pathway and of mechanotransduction to myelin formation in Schwann cells.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Yap and Taz expression and activation during Schwann cell development.
Figure 2: Laminins and mechanical stimulation regulate Yap and Taz in primary Schwann cells.
Figure 3: Ablation of Taz in Schwann cells impairs radial sorting of axons.
Figure 4: Radial sorting defects in Taz cKO–Yap cHet nerves are associated with a reduction in Schwann cell proliferation at P3.
Figure 5: Taz and Yap control expression of integrin α6 and dystroglycan in Schwann cells.
Figure 6: RNA-seq analysis of Taz cKO–Yap cHet sciatic, brachial and peripheral trigeminal nerves at P3.
Figure 7: Laminin expression and basal lamina organization in Taz cKO and Taz cKO–Yap cHet nerves.

Similar content being viewed by others

Accession codes

Primary accessions

Gene Expression Omnibus

References

  1. Dupont, S. et al. Role of YAP/TAZ in mechanotransduction. Nature 474, 179–183 (2011).

    CAS  PubMed  Google Scholar 

  2. Zhao, B. et al. TEAD mediates YAP-dependent gene induction and growth control. Genes Dev. 22, 1962–1971 (2008).

    CAS  PubMed  PubMed Central  Google Scholar 

  3. Zhang, H. et al. TEAD transcription factors mediate the function of TAZ in cell growth and epithelial-mesenchymal transition. J. Biol. Chem. 284, 13355–13362 (2009).

    CAS  PubMed  PubMed Central  Google Scholar 

  4. Webster, H.D., Martin, R. & O'Connell, M.F. The relationships between interphase Schwann cells and axons before myelination: a quantitative electron microscopic study. Dev. Biol. 32, 401–416 (1973).

    CAS  PubMed  Google Scholar 

  5. Jessen, K.R., Mirsky, R. & Lloyd, A.C. Schwann cells: development and role in nerve repair. Cold Spring Harb. Perspect. Biol. 7, a020487 (2015).

    PubMed  PubMed Central  Google Scholar 

  6. Svaren, J. & Meijer, D. The molecular machinery of myelin gene transcription in Schwann cells. Glia 56, 1541–1551 (2008).

    PubMed  PubMed Central  Google Scholar 

  7. Feltri, M.L., Poitelon, Y. & Previtali, S.C. How Schwann cells sort axons: new concepts. Neuroscientist 22, 252–265 (2015).

    PubMed  Google Scholar 

  8. Halder, G., Dupont, S. & Piccolo, S. Transduction of mechanical and cytoskeletal cues by YAP and TAZ. Nat. Rev. Mol. Cell Biol. 13, 591–600 (2012).

    CAS  PubMed  Google Scholar 

  9. Taveggia, C. et al. Neuregulin-1 type III determines the ensheathment fate of axons. Neuron 47, 681–694 (2005).

    CAS  PubMed  PubMed Central  Google Scholar 

  10. Engler, A.J., Sen, S., Sweeney, H.L. & Discher, D.E. Matrix elasticity directs stem cell lineage specification. Cell 126, 677–689 (2006).

    CAS  PubMed  Google Scholar 

  11. Reginensi, A. et al. Yap- and Cdc42-dependent nephrogenesis and morphogenesis during mouse kidney development. PLoS Genet. 9, e1003380 (2013).

    CAS  PubMed  PubMed Central  Google Scholar 

  12. Feltri, M.L. et al. P0-Cre transgenic mice for inactivation of adhesion molecules in Schwann cells. Ann. NY Acad. Sci. 883, 116–123 (1999).

    CAS  PubMed  Google Scholar 

  13. Feltri, M.L. et al. Conditional disruption of β1 integrin in Schwann cells impedes interactions with axons. J. Cell Biol. 156, 199–209 (2002).

    CAS  PubMed  PubMed Central  Google Scholar 

  14. Benninger, Y. et al. Essential and distinct roles for Cdc42 and Rac1 in the regulation of Schwann cell biology during peripheral nervous system development. J. Cell Biol. 177, 1051–1061 (2007).

    CAS  PubMed  PubMed Central  Google Scholar 

  15. Grinspan, J.B., Marchionni, M.A., Reeves, M., Coulaloglou, M. & Scherer, S.S. Axonal interactions regulate Schwann cell apoptosis in developing peripheral nerve: neuregulin receptors and the role of neuregulins. J. Neurosci. 16, 6107–6118 (1996).

    CAS  PubMed  PubMed Central  Google Scholar 

  16. Vassilev, A., Kaneko, K.J., Shu, H., Zhao, Y. & DePamphilis, M.L. TEAD/TEF transcription factors utilize the activation domain of YAP65, a Src/Yes-associated protein localized in the cytoplasm. Genes Dev. 15, 1229–1241 (2001).

    CAS  PubMed  PubMed Central  Google Scholar 

  17. Hung, H.A., Sun, G., Keles, S. & Svaren, J. Dynamic regulation of Schwann cell enhancers after peripheral nerve injury. J. Biol. Chem. 290, 6937–6950 (2015).

    CAS  PubMed  PubMed Central  Google Scholar 

  18. Lopez-Anido, C. et al. Differential Sox10 genomic occupancy in myelinating glia. Glia 63, 1897–1914 (2015).

    PubMed  PubMed Central  Google Scholar 

  19. Garratt, A.N., Voiculescu, O., Topilko, P., Charnay, P. & Birchmeier, C. A dual role of erbB2 in myelination and in expansion of the schwann cell precursor pool. J. Cell Biol. 148, 1035–1046 (2000).

    CAS  PubMed  PubMed Central  Google Scholar 

  20. Guo, L., Moon, C., Zheng, Y. & Ratner, N. Cdc42 regulates Schwann cell radial sorting and myelin sheath folding through NF2/merlin-dependent and independent signaling. Glia 61, 1906–1921 (2013).

    PubMed  PubMed Central  Google Scholar 

  21. Topilko, P. et al. Krox-20 controls myelination in the peripheral nervous system. Nature 371, 796–799 (1994).

    CAS  PubMed  Google Scholar 

  22. Kuhlbrodt, K., Herbarth, B., Sock, E., Hermans-Borgmeyer, I. & Wegner, M. Sox10, a novel transcriptional modulator in glial cells. J. Neurosci. 18, 237–250 (1998).

    CAS  PubMed  PubMed Central  Google Scholar 

  23. Liu-Chittenden, Y. et al. Genetic and pharmacological disruption of the TEAD-YAP complex suppresses the oncogenic activity of YAP. Genes Dev. 26, 1300–1305 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  24. Pellegatta, M. et al. α6β1 and α7β1 integrins are required in Schwann cells to sort axons. J. Neurosci. 33, 17995–18007 (2013).

    CAS  PubMed  PubMed Central  Google Scholar 

  25. Srinivasan, R. et al. Genome-wide analysis of EGR2/SOX10 binding in myelinating peripheral nerve. Nucleic Acids Res. 40, 6449–6460 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  26. Anbanandam, A. et al. Insights into transcription enhancer factor 1 (TEF-1) activity from the solution structure of the TEA domain. Proc. Natl. Acad. Sci. USA 103, 17225–17230 (2006).

    CAS  PubMed  PubMed Central  Google Scholar 

  27. van der Flier, A. & Sonnenberg, A. Function and interactions of integrins. Cell Tissue Res. 305, 285–298 (2001).

    CAS  PubMed  Google Scholar 

  28. Previtali, S.C. et al. Expression of laminin receptors in Schwann cell differentiation: evidence for distinct roles. J. Neurosci. 23, 5520–5530 (2003).

    CAS  PubMed  PubMed Central  Google Scholar 

  29. Berti, C. et al. Nonredundant function of dystroglycan and β1 integrins in radial sorting of axons. Development 138, 4025–4037 (2011).

    CAS  PubMed  PubMed Central  Google Scholar 

  30. Subramanian, A. et al. Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles. Proc. Natl. Acad. Sci. USA 102, 15545–15550 (2005).

    CAS  PubMed  PubMed Central  Google Scholar 

  31. Horton, J.D. et al. Combined analysis of oligonucleotide microarray data from transgenic and knockout mice identifies direct SREBP target genes. Proc. Natl. Acad. Sci. USA 100, 12027–12032 (2003).

    CAS  PubMed  PubMed Central  Google Scholar 

  32. Leblanc, S.E. et al. Regulation of cholesterol/lipid biosynthetic genes by Egr2/Krox20 during peripheral nerve myelination. J. Neurochem. 93, 737–748 (2005).

    CAS  PubMed  Google Scholar 

  33. Le, N. et al. Analysis of congenital hypomyelinating Egr2Lo/Lo nerves identifies Sox2 as an inhibitor of Schwann cell differentiation and myelination. Proc. Natl. Acad. Sci. USA 102, 2596–2601 (2005).

    CAS  PubMed  PubMed Central  Google Scholar 

  34. Chang, C. et al. A laminin 511 matrix is regulated by TAZ and functions as the ligand for the α6Bβ1 integrin to sustain breast cancer stem cells. Genes Dev. 29, 1–6 (2015).

    PubMed  PubMed Central  Google Scholar 

  35. Lopez-Fagundo, C., Bar-Kochba, E., Livi, L.L., Hoffman-Kim, D. & Franck, C. Three-dimensional traction forces of Schwann cells on compliant substrates. J. R. Soc. Interface 11, 20140247 (2014).

    PubMed  PubMed Central  Google Scholar 

  36. Jagielska, A. et al. Mechanical environment modulates biological properties of oligodendrocyte progenitor cells. Stem Cells Dev. 21, 2905–2914 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  37. Irvine, K.D. & Harvey, K.F. Control of organ growth by patterning and Hippo signaling in Drosophila. Cold Spring Harb. Perspect. Biol. 7, a019224 (2015).

    PubMed  PubMed Central  Google Scholar 

  38. Zanconato, F. et al. Genome-wide association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth. Nat. Cell Biol. 17, 1218–1227 (2015).

    CAS  PubMed  PubMed Central  Google Scholar 

  39. Guo, L. & Teng, L. YAP/TAZ for cancer therapy: opportunities and challenges (review). Int. J. Oncol. 46, 1444–1452 (2015).

    CAS  PubMed  Google Scholar 

  40. Kim, M., Kim, T., Johnson, R.L. & Lim, D.S. Transcriptional co-repressor function of the Hippo pathway transducers YAP and TAZ. Cell Rep. 11, 270–282 (2015).

    CAS  PubMed  Google Scholar 

  41. Aragona, M. et al. A mechanical checkpoint controls multicellular growth through YAP/TAZ regulation by actin-processing factors. Cell 154, 1047–1059 (2013).

    CAS  PubMed  Google Scholar 

  42. Anliker, B. et al. Lysophosphatidic acid (LPA) and its receptor, LPA1, influence embryonic schwann cell migration, myelination, and cell-to-axon segregation. Glia 61, 2009–2022 (2013).

    PubMed  PubMed Central  Google Scholar 

  43. Grigoryan, T. et al. Wnt/Rspondin/β-catenin signals control axonal sorting and lineage progression in Schwann cell development. Proc. Natl. Acad. Sci. USA 110, 18174–18179 (2013).

    CAS  PubMed  PubMed Central  Google Scholar 

  44. Petersen, S.C. et al. The adhesion GPCR GPR126 has distinct, domain-dependent functions in Schwann cell development mediated by interaction with laminin-211. Neuron 85, 755–769 (2015).

    CAS  PubMed  PubMed Central  Google Scholar 

  45. Chen, Z.L. & Strickland, S. Laminin γ1 is critical for Schwann cell differentiation, axon myelination, and regeneration in the peripheral nerve. J. Cell Biol. 163, 889–899 (2003).

    CAS  PubMed  PubMed Central  Google Scholar 

  46. McKee, K.K. et al. Schwann cell myelination requires integration of laminin activities. J. Cell Sci. 125, 4609–4619 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  47. Grove, M. & Brophy, P.J. FAK is required for Schwann cell spreading on immature basal lamina to coordinate the radial sorting of peripheral axons with myelination. J. Neurosci. 34, 13422–13434 (2014).

    PubMed  PubMed Central  Google Scholar 

  48. Schwartz, M.A. Integrins and extracellular matrix in mechanotransduction. Cold Spring Harb. Perspect. Biol. 2, a005066 (2010).

    CAS  PubMed  PubMed Central  Google Scholar 

  49. Paavola, K.J., Sidik, H., Zuchero, J.B., Eckart, M. & Talbot, W.S. Type IV collagen is an activating ligand for the adhesion G protein-coupled receptor GPR126. Sci. Signal. 7, ra76 (2014).

    PubMed  PubMed Central  Google Scholar 

  50. Chance, P.F. et al. DNA deletion associated with hereditary neuropathy with liability to pressure palsies. Cell 72, 143–151 (1993).

    CAS  PubMed  Google Scholar 

  51. Quattrini, A. et al. Beta 4 integrin and other Schwann cell markers in axonal neuropathy. Glia 17, 294–306 (1996).

    CAS  PubMed  Google Scholar 

  52. Gokey, N.G., Srinivasan, R., Lopez-Anido, C., Krueger, C. & Svaren, J. Developmental regulation of microRNA expression in Schwann cells. Mol. Cell. Biol. 32, 558–568 (2012).

    CAS  PubMed  PubMed Central  Google Scholar 

  53. Colombelli, C. et al. Perlecan is recruited by dystroglycan to nodes of Ranvier and binds the clustering molecule gliomedin. J. Cell Biol. 208, 313–329 (2015).

    PubMed  PubMed Central  Google Scholar 

  54. Tse, J.R. & Engler, A.J. Preparation of hydrogel substrates with tunable mechanical properties. Curr. Protoc. Cell Biol. 10, 10.16 (2010).10.1002/0471143030.cb1016s47

    Article  Google Scholar 

  55. Zhao, R., Chen, C.S. & Reich, D.H. Force-driven evolution of mesoscale structure in engineered 3D microtissues and the modulation of tissue stiffening. Biomaterials 35, 5056–5064 (2014).

    CAS  PubMed  PubMed Central  Google Scholar 

  56. Toda, K., Small, J.A., Goda, S. & Quarles, R.H. Biochemical and cellular properties of three immortalized Schwann cell lines expressing different levels of the myelin-associated glycoprotein. J. Neurochem. 63, 1646–1657 (1994).

    CAS  PubMed  Google Scholar 

  57. Jones, E.A. et al. Distal enhancers upstream of the Charcot-Marie-Tooth type 1A disease gene PMP22. Hum. Mol. Genet. 21, 1581–1591 (2012).

    CAS  PubMed  Google Scholar 

  58. Heinz, S. et al. Simple combinations of lineage-determining transcription factors prime cis-regulatory elements required for macrophage and B cell identities. Mol. Cell 38, 576–589 (2010).

    CAS  PubMed  PubMed Central  Google Scholar 

  59. Robinson, M.D., McCarthy, D.J. & Smyth, G.K. edgeR: a Bioconductor package for differential expression analysis of digital gene expression data. Bioinformatics 26, 139–140 (2010).

    CAS  PubMed  Google Scholar 

Download references

Acknowledgements

We thank E. Hurley for technical assistance; A. Sonnenberg (Netherlands Cancer Institute), D. Meijer and P. Brophy (Centre for Neuroregeneration, Edinburgh), the late G. Tarone (University of Turin), L. Sorokin (University of Muenster) and M. Wegner (Friedrich-Alexander University Erlangen–Nürnberg) for antibodies, and the late R. Quarles (National Institute of Neurological Diseases and Stroke) for the S16 cells. This work was funded by grants NS045630 (to M.L.F.), NS096104 (to L.W.) and NS075269 (to J.S.).

Author information

Authors and Affiliations

  1. Department of Biochemistry, Hunter James Kelly Research Institute, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York, USA

    Yannick Poitelon, Kathleen Catignas, Caterina Berti, Marilena Palmisano, Courtney Williamson, Dominique Ameroso, Kansho Abiko, Yoonchan Hwang, Lawrence Wrabetz & Maria Laura Feltri

  2. Waisman Center, University of Wisconsin–Madison, Madison, Wisconsin, USA

    Camila Lopez-Anido & John Svaren

  3. Lunenfeld–Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada

    Alex Gregorieff & Jeffrey L Wrana

  4. Department of Biomedical Engineering, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York, USA

    Mohammadnabi Asmani & Ruogang Zhao

  5. Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York, USA

    Fraser James Sim

  6. Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York, USA

    Lawrence Wrabetz & Maria Laura Feltri

Authors
  1. Yannick Poitelon
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Camila Lopez-Anido
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Kathleen Catignas
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Caterina Berti
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Marilena Palmisano
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Courtney Williamson
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Dominique Ameroso
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Kansho Abiko
    View author publications

    You can also search for this author in PubMed Google Scholar

  9. Yoonchan Hwang
    View author publications

    You can also search for this author in PubMed Google Scholar

  10. Alex Gregorieff
    View author publications

    You can also search for this author in PubMed Google Scholar

  11. Jeffrey L Wrana
    View author publications

    You can also search for this author in PubMed Google Scholar

  12. Mohammadnabi Asmani
    View author publications

    You can also search for this author in PubMed Google Scholar

  13. Ruogang Zhao
    View author publications

    You can also search for this author in PubMed Google Scholar

  14. Fraser James Sim
    View author publications

    You can also search for this author in PubMed Google Scholar

  15. Lawrence Wrabetz
    View author publications

    You can also search for this author in PubMed Google Scholar

  16. John Svaren
    View author publications

    You can also search for this author in PubMed Google Scholar

  17. Maria Laura Feltri
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

Y.P., K.C., C.B., M.P. and M.L.F. designed research and interpreted data; Y.P. performed experiments with assistance from C.L.-A., K.C., C.B., M.P., C.W., D.A., K.A. and Y.H.; C.L.-A. and J.S. designed and performed ChIP sequencing and promoter analysis. M.A. and R.Z. designed and helped to perform biomechanical experiments; A.G. and J.L.W. and L.W. contributed analytical tools; F.J.S. analyzed RNA-seq data; Y.P. and M.L.F. wrote the manuscript; Y.P., C.L.-A., R.Z., F.J.S., J.S., L.W. and M.L.F. analyzed data and critically reviewed the manuscript.

Corresponding author

Correspondence to Maria Laura Feltri.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Integrated supplementary information

Supplementary Figure 1 Schwann cell proliferation and apoptosis are not affected by Taz or Yap ablation at P20.

(a) TUNEL staining (red), pH3 staining (green) and DAPI (blue) analysis on longitudinal section of sciatic nerves from control, Taz and Yap mutants at P20. Scale bar, 100 µm. At least three animals per genotypes were analyzed. (b) Relative number of TUNEL and pH3 positive nuclei, density of nuclei (number of nuclei per mm2 of sciatic nerve) and total number of nuclei in sciatic nerve (length of sciatic nerve measured: 400 μm). The number of Schwann cells is decreased in double mutants. The increase of nuclei density in Taz cKO; Yap cHet and Yap/Taz cKO is likely caused by absence of myelin. n = 6 control mice, 3 Taz cKO, 4 Yap cKO, 4 Taz cKO Yap cHet, 5 Yap cKO Taz cHet; 3 Taz and Yap cKO. One way ANOVA TUNEL P = 0.4768 F (5, 15) = 0.9519 Taz cKO Yap cHet P = 0.1125; One way ANOVA nuclei per mm2 P < 0.0001, F (5, 18) = 18.54 with Bonferroni post hoc test Taz cKO P = 0.2804; Taz cKO Yap cHet P = 0.0002, Taz and Yap cKO Yap cHet P = 0.0062. Two-tailed unpaired Student's t test Taz and Yap cKO nuclei number P = 0.05. Error bars indicate s.e.m. * P < 0.05, ** P < 0.01, *** P < 0.001.

Supplementary Figure 2 The phenotypes of Yap and Taz cKO mice are not due to reduced expression of ErbB2, Cdc42, Egr2 or Sox10 in vivo.

(a) H3K27ac ChIP-Seq enrichment profiles in P15 rat sciatic nerve near (i) Erbb2, (ii) Cdc42, (iii) Egr2 and (iv) Sox10. H3K27ac regions were used to identify the presence of Tead motifs (vertical black bars). (b) Relative mRNA levels in primary rat Schwann cells treated with Verteporfin. Expression of ErbB2, Cdc42 and Sox10 are decreased upon Verteprofin treatment. Error bars indicate s.d. n = 3 independent experiments. Two way ANOVA P < 0.0001, F (2, 24) = 40.96 with Bonferroni post hoc test Erbb2 2 µM P = 0.0136, Erbb2 10 µM P < 0.0001, Cdc42 2 µM P = 0.2804, Cdc42 10 µM P < 0.0001, Egr2 2 µM P = 0.0134, Egr2 10 µM P < 0.0001, Sox10 2 µM P = 0.2312, Sox10 10 µM P < 0.0001. * P < 0.05, **** P < 0.0001. A logarithmic scale was used the y-axis and the origin was set to 1. (c-d) mRNA c) and protein d) levels in control, Taz cKO and Taz cKO; Yap cHet. Expression of Cdc42, ErbB2, Egr2 or Sox10 are not affected in vivo in the mutants. Error bars indicate s.e.m. n=3 (animal). n = 3 mice; One way ANOVA Cdc42 P = 0.3437, Dag1 F (2, 6) = 1.283 with Bonferroni post hoc test Taz cKO Yap cHet P = 0.3454; One way ANOVA ErbB2 P = 0.4162, F (2, 6) = 1.012 with Bonferroni post hoc test Taz cKO Yap cHet P = 0.476. A logarithmic scale was used the y-axis and the origin was set to 1. The western blots were cropped and the complete blots are presented in Supplementary Figure 4.

Supplementary Figure 3 Itga6 is regulated by Yap and Taz with Tead.

(a) H3K27ac ChIP-Seq enrichment profiles in P15 rat sciatic nerve near (i) Itga6 and (ii) Dag1. H3K27ac regions were used to identify the presence of Tead motifs (vertical black bars). (b) ChIP-qPCR analysis on S16 Schwann cells. Enrichments are compared to goat IgG. The negative control site for ChIP-qPCR is a region 17.8 kb from the Tekt3 gene, which is not expressed in Schwann cells. Error bars indicate s.d. n=3 n = 3 independent experiments. Two way ANOVA P < 0.0001 F (2, 42) = 37.94 with Bonferroni post hoc test Sox10 – 20 kb P < 0.0001, Tead1 – 20 kb P < 0.0001, Sox10 – 7.6 kb P = 0.0026, Sox10 + 30 bp P < 0.0001. ** P < 0.01, **** P < 0.0001.

Supplementary Figure 4 Uncropped pictures of the Western blots shown in the manuscript.

Supplementary Figure 5 Microscopy equipment and settings.

Supplementary information

Supplementary Text and Figures

Supplementary Figures 1–5 (PDF 1271 kb)

Supplementary Methods Checklist (PDF 418 kb)

Supplementary Table 1

Genes differentially expressed in Taz cKO–Yap cHet with a false discovery rate of 5% or lower. (XLSX 206 kb)

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Poitelon, Y., Lopez-Anido, C., Catignas, K. et al. YAP and TAZ control peripheral myelination and the expression of laminin receptors in Schwann cells. Nat Neurosci 19, 879–887 (2016). https://doi.org/10.1038/nn.4316

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nn.4316

This article is cited by

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing