Hematopoietic defect in Arid3a KO embryos is rescued by IFN-α. (A) Microarray analysis of transcription factors upregulated by IFN-α in vivo in adult HSCs reveals Arid3a (GSE14361). (B) Immunoblot of Arid3a in the AGM, YS, and PLA. (C) Percentage of Arid3a+ cells in the various VE-cadherin/CD45 compartments showing abundance of Arid3a in hematopoietic cells. Sorted cells were cytospun and stained for Arid3a; n = 4-5. (D) Microarray analysis showing the presence of Arid3a expression in AGM HSCs (VE-cadherin+CD45+) (GSE37000) via presence/absence call. Dotted line indicates the presence/absence cutoff. (E) Boxplot quantification of nuclear Runx1+ surrounding the dorsal aorta in the E10.5 AGM of Arid3a+/+ and −/− sections; n = 13-19. (F) Boxplot quantification of nuclear Runx1+ surrounding the dorsal aorta in the E11.5 AGM of Arid3a+/+, +/−, and −/− sections; n = 6-9. (G) CFU assays from E11.5 Arid3a WT and KO AGMs; n = 3. Error bars indicate standard error of the mean (SEM). (H) Boxplots of donor chimerisms of Arid3a+/+, +/−, and −/− E11.5 to E12.5 AGMs transplanted at 1 e.e. and analyzed at 6, 10, and 14 weeks posttransplantation; 5 × 105 splenic helper cells were used. (I) Boxplots of donor chimerisms of E11.5 Arid3a+/+, +/−, and −/− AGMs transplanted at 0.5 e.e. and analyzed at 6, 12, and 16 weeks posttransplantation. Two-way ANOVA was performed. Statistical significance: *P < .05; **P < .01; ***P < .001. PLA, placenta; YS, yolk sac.