The ability of Meis1 to promote FL-dependent proliferation correlates precisely with its ability to induce leukemogenesis. (A) Location of Meis1 mutations. Point mutations are shown in panel C. (B) Interaction between Meis1a and Pbx1a in the absence of DNA, demonstrated by coimmunoprecipitation. (C) Top panel shows designation of point mutant of Meis1 within the M1 and M2 alpha helices. An asterisk indicates the position of leucine or isoleucine. Bottom panel shows C-terminal sequences of Meis1, Meis2, Meis3, and Prep1 that lie downstream of homeodomain. The 3 repeated motifs are underlined. (D) Interaction between Meis1a and Pbx1a on DNA, demonstrated by EMSA. (E) Expression of Meis1 and Hoxa9 in primary Lin^- marrow cells following retroviral infection and selection for G418 resistance. (F) FL-dependent proliferation demonstrating the requirement for C-terminal residues upstream of amino acid position 370. (G) FL-dependent proliferation demonstrating the importance of interaction with Pbx. Error bars in panels F and G indicate standard deviation of data from repeated experiments. (H) The ability of Meis1 to cooperate with Hoxa9 to cause AML correlates precisely with its ability to evoke FL-dependent proliferation.