Pexophagy and mitophagy in cellular homeostasis, aging and disease

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Peroxisomes are highly plastic organelles involved in several metabolic processes, including fatty acid oxidation, ether lipid synthesis, and redox homeostasis. The number of peroxisomes and their activity dynamically changes in response to nutrient availability and cellular stress. Damaged or superfluous peroxisomes are removed mainly by pexophagy, the selective autophagic degradation of peroxisomes promoted by ubiquitylation of peroxisomal membrane proteins. In this collaborative project, we will investigate molecular mechanisms that control pexophagy and delineate the impact of autophagy-dependent peroxisomal quality control and dynamics on cellular homeostasis, aging and disease. In addition, we will study how the interplay between peroxisomes and mitochondria contribute to safeguarding homeostasis of both organelles. To accomplish these aims, we will combine expertise of the Eimer and Bremm groups as well as the advantages of the respectively used model systems (C. elegans and human cells).    

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