Abstract
Presentation Description :
Mitochondria are dynamic organelles that undergo fission-fusion events to modulate organelle size in response to cellular energy demands, and to remove expired or damaged regions. During apoptosis, the balance of this equilibrium shifts to predominantly fission as part of the cellular degradative process. Pro-apoptotic proteins of the BCL2 gene family, such as BAX, are important mediators of mitochondrial dynamics. In healthy cells, BAX plays an essential role in mitochondrial fusion. During apoptosis, BAX recruitment and oligomerization occurs at mitochondrial foci. Early in this process, BAX forms pores in the mitochondrial outer membrane, which facilitates the release of pro-apoptotic molecules such as cytochrome c and SMAC. Later, however, these foci become the sites of mitochondrial fission. Kinetic studies show that fission coincides with the completion of BAX recruitment. Similarly, mitochondria in cells expressing BAX mutants that can participate in fusion, but not apoptosis, are resistant to fission events after the induction of cell death. This presentation will summarize the current understanding of the cellular machinery that regulates mitochondrial dynamics in the context of the roles played by the pro-apoptotic BAX protein.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.