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Fig. 1
Loss of nr2f1b and isl2 causes vascular defects, and transcriptome analysis identified genes regulated by Nr2f1b and/or Isl2. (A–C,A′–C′) knockdown of isl2 or nr2f1b causes ISV growth stalling in the middle line of the somite, a reduction of the ISV endothelial cells, (B,C) and a mis-patterned vessel plexus at the CVP (B′,C′) at 30–32 hpf when compared to wt controls (A,A′). (D,E) Microarray data analysis in Venn diagrams show that there were 308 and 168 genes upregulated at isl2 MO and nr2f1b MO, respectively, compared to wt, as well as 121 overlapping genes in both isl2 MO and nr2f1b MO when compared to the wild type (D). (E) For the repression targets, 108 and 89 genes are downregulated at isl2 MO and nr2f1b MO, respectively, compared to wt, and 23 genes are overlapped. (F) Functional analysis showed many genes involved in cell cycle regulation, signaling, transporter/channels, transcription, cell communication and protein–protein interactions. (ISV, intersegmental vessel; DLAV, dorsal longitudinal anastomotic vessel; DA, dorsal aorta; PCV, posterior cardinal vein; CVP, caudal vein plexus). Scale bars represent 100 μm.