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. Author manuscript; available in PMC: 2021 Sep 1.
Published in final edited form as: Dev Biol. 2020 Jul 3;465(1):11–22. doi: 10.1016/j.ydbio.2020.06.007

Figure 2. Overexpression of a constitutively active MAP2K1 construct compensates for a reduction in kdrl and kdr expression and partially rescues angiogenic defects in ets1−/−; etv2 MO embryos.

Figure 2.

(A) qPCR analysis of endothelial genes cdh5, kdrl and kdr in whole embryos at 32 hpf. Note the reduction in kdrl and kdr expression in ets1−/−; etv2−/−embryos compared to etv2−/−embryos (B-F’’) Confocal images of 28 hpf Tg(kdrl:GFP) wildtype, ets1−/−, etv2 MO (0.25 ng), ets1−/−; etv2 MO (0.25 ng) and ets1−/−; etv2 MO; fli1aep:mCh-actMAP2K1 embryos. Note the mild angiogenic defects in etv2 MO (0.25 ng) embryos (D) and more severe defects in ets1−/−; etv2 MO embryos(E). (F-F’’) Split images showing vascular GFP expression (F), mCherry expression from the actMAP2K1 construct (F’) and a merged image with GFP and mCherry (F’’). (G) Quantification of ISVs in embryos from B-F. Note the increase in the number of ISVs in ets1−/−; etv2 MO; fli1aep:mCh-actMAP2K1 embryos compared to the ets1−/−; etv2 MO embryos. *P<0.05, ** P<0.01; n.s – not significant; columns and horizontal bars in dotplots represent mean, error bars represent ± SEM.