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. Author manuscript; available in PMC: 2009 Aug 22.
Published in final edited form as: Mol Cell. 2008 Aug 7;31(4):557–569. doi: 10.1016/j.molcel.2008.07.010

Fig. 7. Opa1-Q297V inhibited apoptosis but not Bax activation.

Fig. 7

a. Bax was activated by Chariot-delivered BimS in 293T cells. 293T cells transfected with pcDNA-Opa1-Q297V (right panels) or untransfected (left panels) were Chariot-loaded with BimS protein in the presence of caspase inhibitor Q-VD for 12 h (lower panels) or left untreated (upper panels). Cells were fixed and stained for nuclei (propidium iodide; red) or activated Bax (6A7 antibody; green) as described in Experimental Procedures. b. Expression of Opa1-Q297V inhibited apoptosis. Cells were treated as in panel a., except that the caspase inhibitor Q-VD was omitted. Cells were fixed after 12 h post Chariot-BimS treatment and TUNEL-stained as in Fig. 6. 18.81% of untransfected cells and 1.19% of transfected cells were TUNEL positive at this time. c. Expression of Opa1-Q297V caused the retention of Opa1 complexes and IMS proteins in mitochondria following BimS treatment. Cells were loaded with BimS and incubated for 24 h in the presence of Q-VD, and the heavy membrane fraction containing mitochondria was isolated and treated with EDC. Samples were Western blotted using antibodies to the indicated proteins.