FIG 8 .

Model illustrating the roles of PML and its SUMOylation in anti-Listeria responses. (1) Infection with Listeria triggers the expression of genes involved in innate immunity. A fraction of these genes are regulated by PML, in an LLO-independent manner. (2) Pore formation in the host plasma membranes by LLO induces Ubc9 degradation and oxidative stress, leading to PML de-SUMOylation, multimerization, and association with the nuclear matrix. We propose that this state of PML is sensed as a danger signal by the cell, which triggers in response the dampening of bacterial replication.