Fig. 5. Normal development is restored by simultaneous deletion of both FADD and RIPK3 in RIPK1^D324A/D324A mice.

Analysis was performed to determine the effect of disrupting FADD-mediated apoptosis. Defects in the three mutant E12.5 embryos of the indicated genotypes are similar, contrasting normal embryos in the wild type control (a). The ruler division in mm is shown to the left of embryos. At two-month age, RIPK1^D324A/D324A RIPK3^−/− FADD^−/− (TM) mice are indistinguishable in appearance (b) and in body weights (c) from the wild type (WT) and RIPK3^−/− FADD^−/− (DKO) control mice. Western blot analysis of total splenocytes confirming presence or absence of RIPK1, RIPK3, and FADD proteins (d). Ponceau S staining (pink) was performed as protein loading and transfer control