Figure 1.
A current working model for the TAG-mediated control of T. gondii infection. Upon invasion and formation of the PV of T. gondii, the ATG12–ATG5-ATG16L1 complex is recruited to the PVM. The complex conjugates the LC3 homologs on the PVM of T. gondii, and the conjugated LC3 homologs on the PVM are activated by IFNG (e.g. post-translational modification of the LC3 homologs or through targeting of additional factors [e.g., ubiquitin18,19] that can work with the LC3 homologs) and then recruit the GKS IRGs (for simplicity, just indicated as IRG in the figure) and GBPs upon their induction by IFNG. GKS IRGs and GBPs on the PVM disrupt the membrane by vesiculation, and T. gondii exposed to cytoplasm upon the PV disintegration gets killed and further activates the immune system.