Koji Okamoto

Maintenance of organellar quality and quantity is critical for cellular homeostasis and adaptation to variable environments. Emerging evidence demonstrates that this kind of control is achieved by selective elimination of organelles via autophagy, termed organellophagy. Organellophagy consists of three key steps: induction, cargo tagging, and sequestration, which involve signaling pathways, organellar landmark molecules, and core autophagy-related proteins, respectively. In addition, posttransla

Autophagy-related degradation selective for mitochondria (mitophagy) is an evolutionarily conserved process that is thought to be critical for mitochondrial quality and quantity control. In budding yeast, autophagy-related protein 32 (Atg32) is inserted into the outer membrane of mitochondria with its N- and C-terminal domains exposed to the cytosol and mitochondrial intermembrane space, respectively, and plays an essential role in mitophagy. Atg32 interacts with Atg8, a ubiquitin-like protein l

The mitochondrion is an organelle that carries out a number of important metabolic processes such as fatty acid oxidation, the citric acid cycle, and oxidative phosphorylation. However, this multitasking organelle also generates reactive oxygen species (ROS), which can cause oxidative stress resulting in self-damage. This type of mitochondrial damage can lead to the further production of ROS and a resulting downward spiral with regard to mitochondrial capability. This is extremely problematic be

Selective degradation of mitochondria is a fundamental process that depends on formation of autophagy-related double-membrane vesicles exclusive to mitochondria, and is thus termed mitophagy. In yeast, mitophagy is induced by a shift from respiration to starvation, or prolonged respiratory growth. Here we show that mitochondrial degradation in yeast also occurs selectively under starvation conditions even without respiration. Induction of mitophagy takes place much later than that of bulk autoph

Degradation of mitochondria is a fundamental process conserved from yeast to humans that utilizes the machinery of autophagy. In contrast to starvation-induced, nonselective autophagy responsible for nutrient recycling, selective autophagy, which involves particular cues and receptors required for induction and cargo recognition, respectively, mediates mitochondria-specific breakdown. Although numerous studies highlight that mitochondria autophagy (mitophagy) contributes to homeostatic control o

Mitophagy is one of the selective autophagy pathways that catabolizes dysfunctional or superfluous mitochondria. Under mitophagy-inducing conditions, mitochondria are labeled with specific molecular landmarks that recruit the autophagy machinery to the surface of mitochondria, enclosed into autophagosomes, and delivered to lysosomes (vacuoles in yeast) for degradation. As damaged mitochondria are the major sources of reactive oxygen species, mitophagy is critical for mitochondrial quality contro

Differentiation of Dictyostelium discoideum cells in suspension culture is reported, using a medium containing glucose, albumin, cyclic AMP, EDTA and streptomycin in a phosphate buffer. Production of UDPgalactose:polysaccharide transferase, an enzyme specifically present in prespore cells, and the formation of prespore-specific antigens in more than 60% of the cells, are demonstrated. Differentiation in this medium differs from that previously reported with other suspension systems in that (a) c

Mitophagy is an evolutionarily conserved autophagy pathway that selectively degrades mitochondria. Although it is well established that this degradation system contributes to mitochondrial quality and quantity control, mechanisms underlying mitophagy remain largely unknown. Here, we report that protein N-terminal acetyltransferase A (NatA), an enzymatic complex composed of the catalytic subunit Ard1 and the adaptor subunit Nat1, is crucial for mitophagy in yeast. NatA is associated with the ribo