Figure EV2. RNF144A deficiency impairs DNA virus or exogenous cytosolic DNA‐triggered innate immune responses in PMs.

• A
  Wild‐type (WT) and Rnf144a‐deficient (KO) PMs were infected with HSV‐1 (MOI = 1) for 24 h. The titers of HSV‐1 were determined by standard plaque assay.
• B
  Wild‐type (WT) and Rnf144a‐deficient (KO) PMs were infected with HSV‐1 (MOI = 1) for 8 h. The cells were lysed for real‐time PCR assays.
• C
  Wild‐type (WT) and Rnf144a‐deficient (KO) PMs were transfected with HSV60 (1 μg/ml), ISD (1 μg/ml), VACV70 (1 μg/ml), or HT‐DNA (1 μg/ml) for 8 h. The cells were lysed for real‐time PCR assays.
• D
  Wild‐type (WT) and Rnf144a‐deficient (KO) PMs were infected with HSV‐1 (MOI = 1) for 24 h. The supernatants were collected and subjected to ELISA assays.
• E, F
  Wild‐type (WT) and Rnf144a‐deficient (KO) PMs were infected with HSV‐1 (MOI = 1) (E) or transfected with HSV60 (1 μg/ml) (F) for the indicated periods. Native‐PAGE and SDS–PAGE assays were then performed.
• G
  Wild‐type (WT) and Rnf144a‐deficient (KO) PMs were infected with HSV‐1 (MOI = 1) for the indicated periods. Native‐PAGE and SDS–PAGE assays were then performed.

Data information: Two‐tailed unpaired Student's t‐test, *P < 0.05, **P < 0.01, ***P < 0.001. Data shown are from two (A, D) or at least three independent biological replicates (B, C, E–G). In (B, C), each data point represents a technical replicate. In (A, D), each data point represents an independent biological replicate. Error bars are presented as mean ± SD.

Source data are available online for this figure.