Mitochondria are central hubs for cellular stress adaptation, with their function integrated with both apoptosis and autophagy pathways that determine cell fate. Alterations in mitochondrial morphology and inter-organellar communication shape these outcomes. In this presentation, I will first provide an educational overview of how mitochondrial dynamics (fusion, fission) intersect with intrinsic apoptosis and mitophagy/autophagy regulation. Particular emphasis will be placed on how live-cell high- and super-resolution microscopy has advanced our understanding of these processes, revealing the spatial and temporal coordination of organelle remodeling under stress. In the second part of the talk, I will highlight recent findings from my laboratory on FATE1 (Fetal and Adult Testis Expressed 1), a cancer/testis antigen aberrantly expressed in cancer cells. Unlike its homolog mitochondrial fission factor (Mff), FATE1 does not promote mitochondrial fragmentation but instead preserves mitochondrial networks and prevents stress-induced breakdown. Given that FATE1 is recognized as a factor promoting cancer cell survival, these activities may be integrated with mechanisms that allow tumor cells to resist apoptosis and maintain their survival under chemotherapies. Together this dual focus will illustrate both fundamental principles of mitochondrial stress responses and a concrete example of how a cancer-selective regulator exploits these pathways for oncogenic advantage.

Learning Objectives:

1. Explain how mitochondrial dynamics influence intrinsic apoptosis and autophagy

2. Describe how advanced live-cell and super-resolution microscopy can be used to study mitochondrial stress responses

3. Analyze how mitochondrial remodeling contributes to cancer cell survival and therapy resistance