MCL1 and infection: Because this translocation is supported by anti-apoptotic Bcl-2-proteins [28] and Mcl-1 is strongly upregulated in Ctr-infected cells, we also tested Mcl-1-deficient cells but found a similarly accelerated diffusion of Bax (Supplementary Fig. 7A), suggesting that rapid diffusion of Bax from mitochondria upon Ctr-infection is Mcl-1-independent.