Loss of OPA1 fusion causes the collapse of the mitochondrial network and promotes apoptosis. Fusion of the inner membrane, mediated by optic atrophy-1 (OPA1), is a stress-sensitive mechanism of mitochondrial dynamic homeostasis, controlled by the OMA1 metalloprotease. The mitochondria of mammalian cells are increasingly understood to be a highly dynamic organellar network, using opposing fission and fusion pathways to homeostatically balance mitochondrial organization and bioenergetic function. OMA1’s role as a key mitochondrial stress-sensitive protease motivates exciting new questions regarding its mechanistic regulation and interactions, as well as its broader importance through involvement in apoptotic, stress response, and developmental pathways. Furthermore, emerging evidence suggests that this proteolytic mechanism may have critical importance for cell developmental programs, particularly in cardiac, neuronal, and stem cell settings. This proteolytic mechanism provides sensitive regulation of organellar structure/function but also engages directly with apoptotic factors as a major mechanism of mitochondrial participation in cellular stress response. When ΔΨ m is lost, L-OPA1 is cleaved to short, fusion-inactive S-OPA1 isoforms by the stress-sensitive OMA1 metalloprotease, causing the mitochondrial network to collapse to a fragmented population of organelles. Crucially, optic atrophy- 1 (OPA1) directly links mitochondrial structure and bioenergetic function: when the transmembrane potential across the inner membrane (ΔΨ m) is intact, long L-OPA1 isoforms carry out fusion of the mitochondrial inner membrane. Fusion allows individual mitochondria to form an interconnected reticular network, while fission divides the network into a collection of vesicular organelles. Maintained as an organellar network distributed throughout the cell, mitochondria respond to cellular stimuli and stresses through highly sensitive structural dynamics, particularly in energetically demanding cell settings such as cardiac and muscle tissues. Mammalian mitochondria are emerging as a critical stress-responsive contributor to cellular life/death and developmental outcomes. 2Clinical Laboratory Sciences/Department of Health and Biomedical Sciences, The University of Texas Rio Grande Valley, Edinburg, TX, United States.1Department of Biology, The University of Texas Rio Grande Valley, Edinburg, TX, United States.Robert Gilkerson 1,2*, Patrick De La Torre 1 and Shaynah St.

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