Figure S2.

Endothelial Kras^G12D or Braf^V600E gain-of-function mutations cause hepatic vascular cavernomas and embryonic lethality in mice. (A and B) Lyve1 (green) and Pecam1 (red) coimmunofluorescent staining with Hoechst nuclear counterstain (blue) on tamoxifen-treated adult Kras^{G12D F/+}; Cdh5^CreERT2 (A) and Braf^{V600E F/+}; Cdh5^CreERT2 (B) liver sections shows contribution of Lyve1⁺ and Pecam1⁺ endothelial cells to hepatic vascular cavernomas (white arrows). n = 3. Scale bars: 100 μm (top row) and 10 µm (bottom row). Two independent experiments. (C and D) Dissected livers and H&E-stained liver frontal sections show vascular cavernomas (black arrows) in tamoxifen-treated Kras^{G12D F/+}; Cdh5^CreERT2 (C) and Braf^{V600E F/+}; Cdh5^CreERT2 (D) neonatal mice. Lyve1 (green) and Pecam1 (red) coimmunofluorescent staining with Hoechst nuclear counterstain (blue) on Kras^{G12D F/+}; Cdh5^CreERT2 (C) and Braf^{V600E F/+}; Cdh5^CreERT2 (D) liver sections shows contribution of Lyve1⁺ and Pecam1⁺ endothelial cells to hepatic vascular cavernomas (white arrows). n = 3. P, postnatal day. Scale bars: 500 μm (top row), 100 µm (second and third rows from top), and 10 µm (bottom row). Two independent experiments. (E and F) Genotyping tables of embryos or pups derived from Kras^{G12D F/+} mice crossed with either Lyve1^Cre/+ (E) or Lyve1^Cre/Cre (F) mice. (G and H) Genotyping tables of embryos derived from Braf^{V600E F/F} (G) or Braf^{V600E F/+} (H) mice crossed with either Lyve1^Cre/+ (G) or Lyve1^Cre/Cre (H) mice. χ² P value 0.94 (E, E13.5), 0.09 (E, P0), 0.0001 (F), 0.857 (G, E11.5), 0.285 (G, E14.5), 1.0 (H). LS, liver sinusoid; PV, portal vein.