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. Author manuscript; available in PMC: 2015 Oct 23.
Published in final edited form as: Nature. 2015 Feb 2;520(7548):553–557. doi: 10.1038/nature14156

Extended Data Figure 7. HSV1 UL12 M185 expression is sufficient to trigger mtDNA stress, TFAM depletion, and antiviral priming in BMDM; infection with UL12-deficient HSV-1 fails to induce mtDNA stress, elicits lower vaginal type I interferon responses, and spreads more readily to DRG.

Extended Data Figure 7

a, WT BMDM were transduced with HSV1 UL12 M185 expressing or empty retroviruses (RV) and relative mtDNA abundance, protein expression, and ISG mRNA expression determined. b, WT MEFs were infected HSV1 (UL12-FLAG) or UL12-deficient HSV1 (UL12Δ + UL98-FLAG) at MOI 10 for 3 hours and analyzed by confocal microscopy. c, WT MEFs were infected HSV1 (UL12-FLAG) or UL12-deficient HSV1 (UL12Δ + UL98-FLAG) at MOI 2 for 24 hours and mtDNA abundance was determined by qPCR. d, The vaginas of WT mice (n=3 per condition) were inoculated with 106 p.f.u. of HSV1 (UL12-FLAG) or UL12-deficient HSV1 (UL12Δ + UL98-FLAG), and 24 hours post infection, vaginal RNA was extracted and gene expression analyzed by qRT-PCR. e, Mice (n=3 per condition) were infected as previously described, and 10 days post infection, DNA from DRG was isolated for mtDNA and HSV-1 genome abundance measurements by qPCR. Error bars indicate ± s.e.m. of triplicates and data are representative of two independent experiments. *=p<0.05, **=p<0.01, ***=p<0.001; unless noted p<0.05, ns=not significant.