Fig. 6. Endothelial progenitors exhibit distinct defects in npas4l, etsrp, tal1, and lmo2 mutants. (A) Generation of etsrp, tal1, and lmo2 mutants containing in-frame or out-of-frame indels. aa, amino acid. (B to D) Numbers of (B) npas4l reporter and Pax2a double-positive cells, (C) all Pax2a-expressing cells, and (D) npas4l reporter–expressing skeletal muscle cells, per field of view (319.45 μm long area over the yolk extension). Cells were counted in 3D confocal lateral views at 24 hpf. Data are represented as individual data points, median, interquartile range, and extremes excluding outliers. P values were calculated by Poisson regression and adjusted to counteract the multiple testing problem. A subset of these data is also shown in Fig. 2 (C to E). (E) Transverse sections of npas4l+/−, npas4l−/−, etsrp−/−, tal1−/−, and lmo2−/− embryos at 24 hpf; endothelial progenitors and endothelial cells outlined by yellow dotted lines. Major axial vessels form in npas4l+/− embryos, while in npas4l−/− embryos, endothelial progenitors fail to migrate or to express the fli1a:GFP reporter. In etsrp−/− embryos, endothelial progenitors migrate but fail to form vessels. In tal1−/− and lmo2−/− embryos, endothelial progenitor migration is partly impaired; the endothelial progenitors that do reach the midline differentiate and express fli1a:GFP. Scale bars, 20 μm.
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