FBS Colloquia No.181Laboratory of Mitochondrial Dynamics

Regulation of mitochondrial clearance via trans-acting factors on the endoplasmic reticulum

Selective clearance of excess or unhealthy mitochondria is a fundamental process conserved from yeast to humans, contributing to mitochondrial quantity and quality control. This catabolic event primarily depends on "autophagy", a cellular self-eating pathway that mediates transport of cytoplasmic components to lysosomes for degradation, and is thus called "mitophagy". Defects in mitophagy are associated with a myriad of disorders such as mitochondrial malfunction, neurodegeneration, heart/liver failure, aging, and cancer, underscoring the physiological relevance. Although previous studies have revealed multiple key molecules that establish the selectivity of mitophagy, how cells coordinate mitochondrial clearance and other cellular functions remains poorly understood. Using budding yeast as a model organism, we provide evidence suggesting an unexpected link between mitophagy and the endoplasmic reticulum protein biogenesis/degradation pathways. Possible mechanisms regulating mitochondrial clearance through the heterologous organellar factors acting in trans will be discussed.