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. Author manuscript; available in PMC: 2013 Mar 15.
Published in final edited form as: Cell Host Microbe. 2012 Mar 15;11(3):290–297. doi: 10.1016/j.chom.2012.01.016

Figure 3. DAI and RIP3 cooperate in virus-induced necrosis.

Figure 3

(A) RIP3 and DAI interaction in the absence of vIRA. IB of immunoprecipitations (IP) and whole cell lysates (WCL; 5% total) showing DAI, M45, RIP3 and β-actin in 3T3-SA cells infected with M45mutRHIM MCMV (MOI=5) harvested at the indicated times (h.p.i.). (B) IB analysis to detect DAI, RIP3, RIP1 and β-actin in 3T3-SA cells transfected with non-targeting (NT) control, DAI, or RIP3 siRNAs (C) Viability of 3T3-SA cells transfected with the indicated siRNA and infected with M45mutRHIM (MOI=10) and treated with DMSO control or Nec-1 inhibitor (30μM). (n=4) (D) IB analysis to detect DAI, RIP3, RIP1, and β-actin in C57BL/6 control, DAI−/−, and RIP3−/− murine embryonic fibroblasts (MEFs) (E) Viability of C57BL/6 control, DAI−/−, and RIP3−/− MEFs infected with M45mutRHIM MCMV (MOI=10)(n=3). (F) Single-step replication of WT and M45mutRHIM MCMV (MOI of 5) on control C57BL/6 (left) and DAI−/− (right) MEFs. Viral titers determined by plaque assay with the first (0 h) time point representing amount of virus in the inoculum. Error bars, SD. *p<0.01, **p<0.001, #not significant (p>0.05). See also related Figure S3.