RESEARCH

Autophagy is an evolutionarily conserved and important process during which our cells digest or cannibalize small parts of themselves.

Autophagy plays an essential role during starvation, the defense against pathogenic microorganisms, the removal of protein aggregates and the degradation of damaged organelles. Misregulated or defective autophagy can result in neurodegeneration and premature aging and is thus highly relevant to a plethora of human diseases.
Autophagy is induced by an upstream signal such as starvation, the detection of pathogenic microorganisms in the cytosol or by damaged mitochondria. This signal triggers the most enigmatic and fascinating step of autophagy, the de novo formation of autophagosomes. Initially a small double membrane bound structure is formed, which grows and adopts the shape of a cup. This cup-shaped structure eventually fuses at its rims to form a double membrane bound organelle enclosing a part of the cell’s cytoplasm. The autophagosome then fuses with components of the classical endosomal system thereby maturing to an autolysosome within which the content is degraded. The degraded content can subsequently be used for the synthesis of factors that are essential for the survival of the cell.
Although many genes that are important for autophagy have been identified we have only a very limited understanding of how this important and fascinating process is regulated and executed. Thus, the challenge now is to assign functions to these genes in order to gain a better understanding of the mechanisms that orchestrate autophagy.
We are a multidisciplinary team employing cell biology, biochemistry, light- and electron microscopy as well as structural biology approaches. Our findings will give important insights into mechanisms of autophagy.