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. Author manuscript; available in PMC: 2016 Dec 23.
Published in final edited form as: Leukemia. 2016 Mar 2;30(6):1375–1387. doi: 10.1038/leu.2016.27

Figure 6.

Figure 6

Development of pre-B acute lymphoblastic leukemia in PU.1, IRF4 or IRF8 compound mutant mice. (A) Representative plots of CD19 and B220 expression from isolated splenocytes of moribund mice (upper panel), and cultured leukemic cells (lower panel) of the indicated genotypes. Data are compared to normal control wild-type splenocytes (WT). (B) Expression of IL-7Rα, IgM and Igκ on the gated CD19+B220− leukemic cells and CD19+B220+ WT B cells from (A). Gray histograms show unstained controls. (C) DNA was extracted from leukemias of indicated genotype and subjected to PCR for Igh VDJ rearrangements with sets of primers recognizing various VH gene families. The amplified samples were run on an agarose gel and the alleles assessed and shown. (D) Leukemic cells of the indicated genotypes were lysed and subjected to western blotting for IgM and Igκ. Actin serves as a control for equal protein loading. WT pre-B cells served as a positive control. Note the Igκ in WT pre-B cells is intracellular. Mouse tumor numbers are indicated. (E) Cultured leukemic cells of the indicated genotypes were lysed and subjected to western blotting for PU.1, IRF4, IRF8 and Pax5. Actin serves as a control for equal protein loading. Symbols in (D) and (E) represent the existence of two (+), one (+/−) or no (−) functional alleles for the indicated genes.