Fig. 6: Hoxa9 rescues HSC self-renewal capacity in Zfp90 deficient mice.
a Zfp90+/+ or Zfp90−/− HSCs were transfected with Hoxa9-overexpressing virus or vehicle and cultured in methocult medium for CFC formation assays. CFU-M, CFU-G, CFU-GM, and BFU-E colonies were counted. Results are shown as the means ± S.D. n = 6 for each group. b Zfp90+/+ or Zfp90−/− BM cells were transfected with Hoxa9-overexpressing virus or vehicle and transplanted into lethally irradiated CD45.1+ mice. After 16 weeks, the chimeras were resolved with BrdU for 3 days, and donor-derived HSCs were analyzed by FACS on day 6. n = 6 for each group. c Numbers of LT-HSCs, ST-HSCs, MPPs, CLPs and CMPs in chimeras from (b). d 5 × 105 Zfp90+/+ or Zfp90−/− BM cells transfected with Hoxa9-overexpressing virus or vehicle were transplanted into lethally irradiated CD45.1+ mice supplemented with 5 × 105 CD45.1+ helper cells for competitive BM transplantation assay. Donor-derived hematopoietic cells in the blood were analyzed via FACS. n = 6 for each group. e A schematic work model. Zfp90 regulates HSC homeostasis via recruiting the NURF complex to initiate Hoxa9 expression. *p<0.05, **p<0.01, and ***p<0.001 by two-tailed Student’s t test. All data presented are shown as the means±SD collected from three independent experiments
