TRIMming down Mycobacterium tuberculosis replication: TRIM32 is required for bacterial ubiquitination and autophagy induction in macrophages

Figures & data

Figure 1. Molecular mechanisms underlying xenophagy response to Mtb infection. Intracellular Mtb replication and survival in macrophages is counteracted by xenophagy-mediated lysosomal degradation. Membrane permeabilization by bacterial effectors makes Mtb-containing vesicles accessible to the autophagy machinery. In this context, Mtb has to be first ubiquitinated to then recruit the SARs of the sequestome 1 (SQSTM1)/P62 family. SARs are both involved in recruiting the autophagy machinery for the in situ formation of the autophagosome (not shown in the picture), and in bacterial engulfment by binding to the autophagosome protein MAP1LC3B (LC3). PARKN, SMURF1, TRIM16 and TRIM32 are E3 ligases mediating Mtb ubiquitination. TRIM32 is also necessary to allow BECN1 translocation onto Mtb-containing vesicles. GAL3: GALECTIN 3. Phagophore: nascent autophagosome. The picture was created with BioRender.com.