Skip to main content
. 2017 Sep 18;8(50):87607–87622. doi: 10.18632/oncotarget.20999

Figure 4. Necdin deficiency decreases the proliferation of hematopoietic progenitor cells expressing AML1-ETO9a.

Figure 4

(A) Fetal liver cells isolated from wild-type (WT) or Necdin knock-out (KO) mice were transduced with retroviruses expressing GFP (MIGR1) or AML1-ETO9a. Representative flow cytometry plots show the frequency of transduced cells (GFP+) 72 hours following transduction. (B) Transduced wild type and Necdin null fetal liver cells (GFP+) were cultured in serum free medium in the presence of cytokines for seven days. The frequency of hematopoietic stem and progenitor cells was determined by flow cytometry analysis. Representative flow cytometry plots show the frequency of Kit+CD11b−Gr1− and Kit+CD11b+Gr1+ cells at 7 days in liquid culture. (C) The frequency of Kit+CD11b−Gr1− and Kit+CD11b+Gr1+ cells in the liquid culture (p<0.2, n=2). (D) Necdin null fetal liver cells expressing AML1-ETO9a show enhanced replating potential compared to WT cells (*p<0.05, **p<0.01, n=3). (E) Liquid culture of WT and Necdin null fetal liver cells expressing AML1-ETO9a. Cell proliferation at 48 hours was determined by cell counting. Cell growth was presented relative to the number of input cells in each group, set as 1 (**p<0.01, n=3). (F) Liquid culture of WT and Necdin null fetal liver cells expressing AML1-ETO9a. Cell proliferation at 72 hours was determined by cell counting. Cell growth was presented relative to the number of input cells in each group, set as 1 (**p<0.01, n=3).