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. Author manuscript; available in PMC: 2016 Feb 16.
Published in final edited form as: Nature. 2015 Jul 23;523(7561):468–471. doi: 10.1038/nature14569

Figure 3. 11,12-EET induces a PI3K-dependent AP-1/runx1 transcriptional program to increase HSPC specification.

Figure 3

a–b, Stable flk1:dnJUNB-2A-GFP expression blocking AP-1 function suppressed 11,12-EET-enhanced HSPCs in the AGM. Representative images of runx1/cmyb in situ hybridization (a) and quantification (b) after 11,12-EET treatment (24–36 hpf). Embryos scored as high, medium, or low runx1/cmyb, summed across 4 experiments. *, p=0.01; ***, p<0.0001 by Chi-square. WT, wild-type. c, Schematic of chemical screen for EET signaling pathway suppressors. d–e,11,12-EET induced AP-1 family transcription factors (fosl2, junb/junbl) (d) and runx1 (e), suppressed by cotreatment with LY294002, a PI3K inhibitor, in the AGM and tail (d–e) (3 independent experiments, n>40). Same images from Fig. 2b as staining controls (e).