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. 2009 Dec 18;11(2):133–138. doi: 10.1038/embor.2009.258

Figure 2.

Figure 2

The RLR signalling pathway is modulated by alterations in mitochondrial dynamics. (A) HeLa cells were transfected with control, Drp1, Fis1, OPA1 or Mfn1 shRNA. After the selection of transfectants, cells were infected with SeV H4 and at various times after infection MAVS, p-IRF3, IRF3, p-IκBα and IκBα were analysed in cell extracts by immunoblotting. Actin was used as a protein loading control. *A probable non-specific protein band. Data shown are representative of three independent experiments. (B,C) IFNβ-Luc or NF-κB-Luc reporter plasmids were transfected into control cells or Drp1-, Fis1-, OPA1- or Mfn1-depleted cells, which were then infected with SeV H4 for 9 h (B) or transfected with poly I:C for 8 h (C), and then IFNβ induction and NF-κB activation were assessed. (D) The same conditions as in panel B, but HeLa cells were replaced by human embryonic kidney 293 cells. **0.001<P<0.01, *0.01<P<0.05. Drp1, dynamin-related protein 1; IFN, interferon; IRF, IFN regulatory factor; Luc, luciferase; MAVS, mitochondrial antiviral signalling; Mfn1, mitofusion 1; NF-κB, nuclear factor-κB; OPA1, optic atrophy type 1; RLR, RIG-I-like receptor; RLU, relative luciferase unit; SeV, Sendai virus; shRNA, short-hairpin RNA.