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. 2017 Sep 15;130(18):3023–3039. doi: 10.1242/jcs.205666

Fig. 6.

Fig. 6.

Mcl-1 degradation promotes mitochondrial dysfunction and neurotoxicity. (A) Mcl-1 ablation is neurotoxic in HT22 cells. Scrambled-shRNA infected, Cdk5-shRNA- infected, Mcl-1-shRNA-infected or roscovitine-exposed HT22 cells were treated with glutamate for 24 h. Cell viability was examined using an MTT assay. *P<0.05, compared with untreated HT22 cells. (B) Ectopic expression of T92A-Mcl-1 rescues cells from glutamate toxicity. HT22, Mcl-1-HT22 and T92A-Mcl-1-HT22 cells were treated with glutamate in the absence or presence of roscovitine and Cdk5 shRNA. Cell viability was examined using an MTT assay. *P<0.05, compared with respective control cells. (C) Glutamate stimulation induces mitochondrial depolarization in HT22 cells. Mitochondrial depolarization was analyzed using JC-1 dye. (D) Glutamate stimulation induces mitochondrial depolarization in Mcl-1-HT22 cells. (E) T92A-Mcl-1-HT22 cells are more resistant to mitochondrial depolarization than control HT22 cells. (F) Ratio of JC-1 aggregates versus monomers in HT22, Mcl-1-HT22 and T92A- Mcl-1-HT22 cells. Data are mean±s.e.m. from three independent experiments. *P<0.05, compared with untreated cells. Scale bars: 20 μm.