Figure 1 | Cell Death & Differentiation

Figure 1

From: Mitochondrial dysfunction triggered by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response

Figure 1

Loss of HtrA2 results in a transcriptional stress response. (a) Rotenone induces a greater number of transcriptional changes in HtrA2 KO cells. Venn diagram representation of the overlap of probe sets regulated by rotenone in WT and HtrA2 KO MEFs. (b) CHOP is upregulated in immortalized HtrA2 KO MEFs by rotenone treatment. Short treatment with rotenone fails to induce CHOP expression in WT cells, whereas it results in approximately twofold induction in HtrA2 KO cells. Prolonged rotenone treatment leads to a more pronounced induction of CHOP in KO MEFs when compared with WT controls. MEFs were treated with vehicle, 25 μM rotenone for 3 h or 10 μM rotenone for 8 h. Transcript levels of CHOP are shown relative to vehicle treatment. Mean values±S.D.; n=3. Statistically significant values (two-tailed unpaired t-test) are indicated. (c) CHOP mRNA is induced by transient downregulation of HtrA2. HtrA2 was downregulated using siRNA in Neuro-2a neuroblastoma cells, and immortalized WT and HtrA2 KO MEFs. Transcript levels of HtrA2 and CHOP are shown relative to control siRNA. Mean values±S.D.; n=3. Statistically significant values (two-tailed unpaired t-test) relative to control siRNA are indicated. ** for P<0.01 and * for P<0.05

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