Figure 2
BCR-ABL increases SSA repair frequency. Changes in SSA repair frequency were determined by flow cytometry in response to I-SceI–induced DSBs in cells left untreated or treated with imatinib (1 μM) for 48 hours using the SAGFP reporter. BaF3 and BaF3.BCR-ABL cells stably (A-B) or transiently (C) expressing the SAGFP reporter were used. GFP+ cells were counted by flow cytometry (A dot plot of typical experiments) and compared with untreated samples (B-C, n = 3). Cellular expression of HA-tagged I-SceI (HA) and actin was detected by immunoblotting, as indicated (B bottom panels). (D) BaF3 cells with inducible BCR-ABL were either left untreated or treated with doxycycline to induce BCR-ABL expression (n = 4). (E) K562 (n = 3) and Meg-01 (n = 4) cells (expressing the BCR-ABL oncogene) as well as HEK293 (n = 4) and COS (n = 3) cells (BCR-ABL–negative) were used to measure SSA frequency, as indicated.

BCR-ABL increases SSA repair frequency. Changes in SSA repair frequency were determined by flow cytometry in response to I-SceI–induced DSBs in cells left untreated or treated with imatinib (1 μM) for 48 hours using the SAGFP reporter. BaF3 and BaF3.BCR-ABL cells stably (A-B) or transiently (C) expressing the SAGFP reporter were used. GFP+ cells were counted by flow cytometry (A dot plot of typical experiments) and compared with untreated samples (B-C, n = 3). Cellular expression of HA-tagged I-SceI (HA) and actin was detected by immunoblotting, as indicated (B bottom panels). (D) BaF3 cells with inducible BCR-ABL were either left untreated or treated with doxycycline to induce BCR-ABL expression (n = 4). (E) K562 (n = 3) and Meg-01 (n = 4) cells (expressing the BCR-ABL oncogene) as well as HEK293 (n = 4) and COS (n = 3) cells (BCR-ABL–negative) were used to measure SSA frequency, as indicated.

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