Figure 5.
Figure 5. Exogenous wt PU.1 promotes differentiation of the PU.1-deficient leukemia cells. (A) Morphology of S1.1 cells infected with wild-type PU.1, mutant PU.1, or the vector and cultured for 4 days with GM-CSF. Cells in which PU.1 has induced a macrophage-like appearance are indicated (arrows). (B) Flow cytometric profiles showing that, in the presence of GM-CSF, wt PU.1 induced more marked expression of the myeloid differentiation markers CD11b (Mac-1) and Gr-1. Numbers indicate percentages of cells in each quadrant. (C) Semiquantitative RT-PCR (5-fold steps) showing that wt PU.1 induced a more striking increase in expression of the mRNAs for CD11b, gp91, M-CSF receptor, and myeloperoxidase (mpo) than the mutant PU.1 and that neither affected expression of G-CSF receptor or hypoxanthine phosphoribosyl transferase (HPRT), a loading control.

Exogenous wt PU.1 promotes differentiation of the PU.1-deficient leukemia cells. (A) Morphology of S1.1 cells infected with wild-type PU.1, mutant PU.1, or the vector and cultured for 4 days with GM-CSF. Cells in which PU.1 has induced a macrophage-like appearance are indicated (arrows). (B) Flow cytometric profiles showing that, in the presence of GM-CSF, wt PU.1 induced more marked expression of the myeloid differentiation markers CD11b (Mac-1) and Gr-1. Numbers indicate percentages of cells in each quadrant. (C) Semiquantitative RT-PCR (5-fold steps) showing that wt PU.1 induced a more striking increase in expression of the mRNAs for CD11b, gp91, M-CSF receptor, and myeloperoxidase (mpo) than the mutant PU.1 and that neither affected expression of G-CSF receptor or hypoxanthine phosphoribosyl transferase (HPRT), a loading control.

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