Figure 5.

Targets of bacteria in ER and mitochondria during infection. Mtb induces ER stress-mediated apoptosis via ROS, calreticulin (CRT), Par-4 (Par4) and Ca²⁺ release. M. avium increases ROS-mediated ER stress, leading to activation of the RIDD pathway. Cholera toxin (CT) of V. cholera phosphorylates IRE1. Helicobacter pylori secretes VacA, leading to activation of PERK and DRP1. L pneumophila and S. flexneri induce mitochondrial fragmentation in a DRP1-dependent manner. Mtb also triggers mitochondrial fragmentation by inhibiting MFN2. Mtb, Mycobacterium tuberculosis; M. avium, Mycobacterium avium; L. monocytogenes, Listeria monocytogenes; H. pylori, Helicobacter pylori; V. cholera, Vibrio cholera; L pneumophila, Legionella pneumophila; S. flexneri, Shigella flexneri. (Created with BioRender.com accessed on 29 March 2021).