Fig. 6: Proposed model for the role of YfiD in the pathogenesis of E. piscicida. | Communications Biology

Fig. 6: Proposed model for the role of YfiD in the pathogenesis of E. piscicida.

From: Type III secretion system effector YfiD inhibits the activation of host poly(ADP-ribose) polymerase-1 to promote bacterial infection

Fig. 6

Upon infection, internalized bacteria-caused DNA lesion is recognized by PARP1 followed by its self-activation. The accumulated PAR leads to enhanced inflammatory response and regulated cell death in the residing macrophages, restraining E. piscicida’s replication in macrophages. Along with the occurrence of DNA damage events, YfiD would be delivered into host cells through T3SS and then translocated into the nucleus, where it interacts with the ART domain of PARP1 to impair PAR formation. This blockade rescues E. piscicida from niche disruption and inflammatory elimination, facilitating E. piscicida proliferation and pathogenicity in the host.

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