Supplementary Materials

Supplementary Materials for:

Inactivating mutations in Drosha mediate vascular abnormalities similar to hereditary hemorrhagic telangiectasia

Xuan Jiang, Whitney L. Wooderchak-Donahue, Jamie McDonald, Prajakta Ghatpande, Mai Baalbaki, Melissa Sandoval, Daniel Hart, Hilary Clay, Shaun Coughlin, Giorgio Lagna, Pinar Bayrak-Toydemir,* Akiko Hata*

*Corresponding author. Email: pinar.bayrak-toydemir{at}aruplab.com (P.B.-T.); akiko.hata{at}ucsf.edu (A.H.)

This PDF file includes:

  • Fig. S1. Drosha morphants develop angiogenesis defects.
  • Fig. S2. Generating Drosha mutant fish by CRISPR/Cas9.
  • Fig. S3. Drosha morphants showed vascular leakiness.
  • Fig. S4. Drosha cKOEC embryos showed mild angiogenesis defects and a sign of hemorrhage.
  • Fig. S5. Drosha cKOEC embryos showed disorganized and dilated vasculature.
  • Fig. S6. Drosha iKOEC mice show vascular leakage.
  • Fig. S7. The distribution of the tight junction protein ZO-1 is disrupted in the endothelial cells of Drosha iKOEC mice.
  • Fig. S8. In vitro processing assay of pri-miR-21 and the BMP-Smad signaling pathway in cells expressing DROSHA mutants or depleted of Drosha.
  • Fig. S9. ISV defects mediated by the knockdown of Drosha by morpholino oligos are rescued by coinjection of wild-type (WT) Drosha mRNA, but not by mutant mRNA.

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Citation: X. Jiang, W. L. Wooderchak-Donahue, J. McDonald, P. Ghatpande, M. Baalbaki, M. Sandoval, D. Hart, H. Clay, S. Coughlin, G. Lagna, P. Bayrak-Toydemir, A. Hata, Inactivating mutations in Drosha mediate vascular abnormalities similar to hereditary hemorrhagic telangiectasia. Sci. Signal. 11, eaan6831 (2018).

© 2018 American Association for the Advancement of Science