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. Author manuscript; available in PMC: 2016 Aug 15.
Published in final edited form as: Dev Biol. 2015 May 22;404(2):49–60. doi: 10.1016/j.ydbio.2015.05.011

Figure 2. plk2b regulates endothelial cell sprouting.

Figure 2

(A–D) Fluorescence micrographs show that loss of plk2b function in Tg(kdrl:mcherry-ras) zebrafish embryos results in underdeveloped intersomitic vessel sprouting (open arrowheads) at 36 hpf. (A) control MO (n = 0/149); (B) plk2b ATG MO (MO1) (n = 125/171); (C) plk2b splice MO (MO2) (n = 89/137); (D) dn-plk2b RNA – dominant negative plk2b (n = 49/85). Injecting (E) 80 pg of plk2b (n = 31/103) or (F) 80 pg of hPLK2 (n = 24/71) can rescue the plk2b MO1 vascular sprouting defect. (G) Injecting 80 pg of plk2b RNA into wild-type Tg(kdrl:mcherry-ras) embryos did not cause any significant vascular phenotypes (n = 0/105). However, (H) injecting 160 pg of plk2b resulted in increased ISV spouting and branches (arrowheads) (n = 91/145). Top, dorsal longitudinal anastomotic vessel (yellow asterisk); bottom, dorsal aorta/cardinal vein. Scale bar, 80 µm. Quantitative measurements of (I) intersomitic vessel length and (J) the number of ISV branches for each corresponding condition. Mean +/− s.e.m. *p<0.05 by ANOVA.