Extended Data Fig. 9: Characterization of direct YAP/TAZ-TEAD target genes in ECs.

a,b, ChIP-seq signals of TAZ, YAP and TEAD1 at the genomic loci of the canonical target genes ANKRD1 (a) and AXL (b). ChIP-seq signals are represented as reads per kilobase per million mapped reads (RPKMs). c,d, Slc7a5 expression in ECs isolated from the lungs of Rosa26-Taz^{S89A fl/fl} (c) or Yap^fl/fl;Taz^fl/fl (d) mice followed by transduction with control (AdCtrl) or Cre-encoding (AdCre) adenoviruses. Slc7a5 transcript levels were determined by RT-qPCR (c, n = 6 independent samples; d, n = 6 independent samples). e, Reduced cell proliferation in SLC7A5-deficient HUVECs (gSLC7A5) as measured by ³H-thymidine DNA incorporation (n = 8 independent samples). Values are represented as fold change relative to control (gCtrl). f, Quantification of vascular parameters in Ctrl and Slc7a5^iEC-KO mice as indicated (EC area: n = 8 (Ctrl) and 10 (Slc7a5^iEC-KO) independent samples; EC number / field: n = 9 (Ctrl) and 11 (Slc7a5^iEC-KO) independent samples; EC proliferation: n = 9 (Ctrl) and 11 (Slc7a5^iEC-KO) independent samples). g, Immunofluorescence staining for EdU, ERG and PECAM in P6 Ctrl and Slc7a5^iEC-KO retinas. h, Confocal images of VECAD, p-S6^Ser235/236 and PECAM stained P6 retinas of Ctrl and Slc7a5^iEC-KO mice, suggesting reduced mTORC1 signaling in Slc7a5 mutants. The isolated p-S6^Ser235/236 signal is shown in grey at the bottom of the panel. i, Immunoblots of HUVECs transduced with Ctrl or SLC7A5 encoding lentivirus, showing that overexpression of SLC7A5 is insufficient to restore mTORC1 activity in YAP/TAZ-depleted HUVECs (siYAP/TAZ). Western blot data in i are from the respective experiment, processed in parallel, and are representative of at least three independent experiments. For c, d, e-f, data represent mean ± s.e.m.; two-tailed unpaired t-test. **P < 0.01; ***P < 0.01; ****P < 0.0001. The numerical data, unprocessed western blots and P values are provided as source data.

Source data