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. 2005 May 26;102(23):8281–8286. doi: 10.1073/pnas.0503326102

Fig. 3.

Fig. 3.

Phenotype of Gα13 endothelial-specific knockout and Gα13-/- embryos. All embryos are Tie2-CreTg/o and had a heartbeat at the time of photography. (A–F) Gross appearance of Gα13+/+ embryos (A and D), Gα13flox/- embryos (B and E), and Gα13-/- embryos (C and F). At E9.5 (A–C), Gα13-/- embryos (C) were significantly delayed compared with control embryos (A); developmental arrest appeared to occur at ≈E8.5 as reported in ref. 17. Gα13 endoKO embryos (B) had turned and appeared arrested at ≈E9.0. By E10.5 (D–F), >80% of Gα13 endoKO embryos (E) were either dead or morphologically abnormal, and all Gα13-/- embryos (F) were dead or grossly abnormal. Dilated pericardial sacs, consistent with cardiovascular failure, were a prominent feature in both. (G–I) Whole-mount X-Gal staining of Tie2-CreTg/o; ROSA26R embryos that were Gα13+/+ (G), Gα13flox/- (H), and Gα13-/- (I); embryos were collected at E9.5. Note that there is more primitive vascular plexus in the head of Gα13 endoKO (H) and global Gα13 nulls (I) compared with the control (G). (Scale bars: 1 mm.)