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. 2010 Apr 30;11(6):459–465. doi: 10.1038/embor.2010.50

Figure 4.

Figure 4

Interactions of Bnip3 and Opa1 induce mitochondrial fragmentation and cell death by distinct mechanisms. (A) Established HeLa Tet-Off cells were induced (+) or not (−) for Opa1 expression during 48 h. For the last 24 h, cells were co-transfected with GFP and either HA–Bnip3 (+) or empty (−) vectors. (B) HeLa cells were transfected for 24 h with GFP and either empty (−) or the indicated wild-type or mutant HA–Bnip3 vectors. (C) Cells were as in (A) and cultured with siRNA to Mfn1 (Mfn1) or the off-target luciferase (luc) during the Opa1 induction period. (D) HeLa cells were cultured under hypoxia (+) or normoxia (−) in the presence of siRNA to Bnip3 or luciferase. Fragmentation occurred rapidly (24 h) and was later (72 h) followed by apoptosis. For each panel, data (mean±s.d. of ⩾3 independent experiments; n⩾200 cells per condition) show quantification of mitochondrial fragmentation (left axis) and of apoptosis (right axis) on observation by fluorescence microscopy after MitoTracker and Hoescht 33258 staining. GFP, green fluorescent protein; HA–Bnip3, haemagglutinin-tagged Bnip3; Mfn, mitofusin; siRNA, short interfering RNA.