Autophagy is an evolutionarily conserved membrane trafficking from the cytoplasm to lysosomes, which was discovered nearly half a century ago. In autophagy, the unique double membrane-bound autophagosomes transiently emerge in the cytoplasm, sequester portion of the cytosol and organelles, and eventually fuse with lysosomes to degrade the contents. In addition to the basic role in nutrient supply under starvation conditions, the process unexpectedly functions in development, longevity, immunity, and suppression of various diseases including tumorigenesis, neurodegeneration, and inflammatory diseases.
My group has been working on unraveling the molecular machinery and roles of mammalian autophagy for the last 16 years. LC3, a first protein we identified, has been widely used as a standard marker for autophagosome. Recently, we have provided new insights into biogenesis of autophagosome, which have been topic of longstanding debate. We propose that autophagosome forms in the ER. Furthermore, we found that autophagy eliminates invading pathogenic bacteria. Now we are focusing on how cells recognize the intracellular bacteria and envelop them specifically by autophagosome. I also would like to introduce our recent finding about a new role of autophagy.