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. Author manuscript; available in PMC: 2015 May 8.
Published in final edited form as: Nat Cell Biol. 2006 Aug 20;8(9):1017–1024. doi: 10.1038/ncb1464

Figure 3.

Figure 3

Hoxa5 is critical for leukaemic transformation by CALM–AF10. (a) RT–PCR analysis of the expression of late Hoxa genes and Bmi-1 in vector control (V) and two independent CALM–AF10 knockdown clones (KD1 and KD2) derived from U937 cells, and in mouse bone-marrow cells derived from second round colonies and transduced by wild-type and OM–LZ deletion CALM–AF10 mutants. Lack of detectable signal for Hoxa9 is not due to primer failure as the same primers detected Hoxa9 expression in MLL–ENL transduced cells. (b) Hoxa5 knockout attenuates the transformation capability of CALM–AF10, but has no effect on that of MLL–AF10. Serial colony-plating assays were performed as in Fig. 2a. The average colony numbers ± s.d. of three independent experiments is shown. Due to embryonic lethality of Hoxa5 knockout in C57B6 strain, the bone-marrow cells used in the assays were derived from Hoxa5 knockout and wild-type littermates of 129Sv/Ev-MF1 strain24.