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. Author manuscript; available in PMC: 2013 Jun 3.
Published in final edited form as: Cell. 2010 May 6;141(4):668–681. doi: 10.1016/j.cell.2010.04.018

Figure 7. Transcription factors that control peroxisomal MAVS signaling.

Figure 7

(A,B) WT, IRF1, IRF3 and IRF5 KO MEFs were infected with VSV at an MOI of 3. After 8h RNA was isolated and analyzed for ISG and Type I IFN expression using nCounter.

(C,D) Immortalized MAVS-KO macrophages were retrovirally transduced with MAVS-WT, -Pex, -Mito and-Cyto for 48 h. The transduction efficiency of each cell population was determined to be 20%–30% as assessed by fluorescence microscopy. Cells were infected with reovirus and at the indicated times, were harvested and RNA was analyzed for expression of Type I IFN (C) and other inflammatory genes (D) using nCounter. See also Figure S5.

(E) Model of organelle specific MAVS signaling in fibroblasts. Peroxisomal MAVS is essential for rapid ISG expression independent of Type I IFN, whereas mitochondrial MAVS induces ISGs with delayed kinetics and primarily dependent on Type I IFN secretion. Therefore peroxisomal MAVS mediates immediate and transient antiviral effects, while mitochondrial MAVS promotes a sustained response later during infection. See also Figure S5.