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. Author manuscript; available in PMC: 2023 Sep 15.
Published in final edited form as: Mol Cell. 2022 Aug 9:S1097-2765(22)00708-0. doi: 10.1016/j.molcel.2022.07.012

Figure 3: Intersection of two stress responses secondary to mitochondrial dysfunction.

Figure 3:

ETC dysfunction triggers OMA1 activation, which cleaves multiple substrates, including OPA1 and DELE1. Initially this activity serves a pro-homeostatic response. Prolonged stress activates the pro-apoptotic arm of the integrated stress response, which converges on BCL2 family proteins to trigger MOMP. Cleavage of OPA1 and dissolution of cristae junctions may act to internally prime mitochondria to commit to apoptosis in response to MOMP.