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An international research team led by Osaka University has identified a new mechanism crucial for the initiation of autophagy, a self-degradation process cells use to eliminate unneeded or damaged components. In recent years, autophagy has also been recognized for its roles in aging and lifespan regulation.

During autophagy, intracellular molecules and structures are sequestered within a membrane-bound structure known as an autophagosome, which is subsequently degraded in lysosomes. It is well-established that the formation of autophagosomes involves the coordinated action of multiple autophagy-related proteins.

Previously, the research group revealed that autophagosome formation takes place on the endoplasmic reticulum membrane in close proximity to mitochondria within cells. They also discovered that the PI3K complex, an autophagy-related protein, is essential for this formation process. The activity of the PI3K complex is controlled by the ULK1 complex.

The ULK1 complex is known to translocate from the cytoplasm to the endoplasmic reticulum membrane, where autophagosomes are formed at the onset of autophagy. However, the underlying mechanism and significance of this process were not fully understood until now.

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