Seminarium Zakładu Biofizyki

Most mitochondrial proteins begin as precursors in the cytosol and are imported into the organelle through specialized translocation channels. If a protein misfolds during this process, it may stall, blocking further import and disrupting mitochondrial function and protein homeostasis. We compared molecular mechanisms handling failed import events in yeast and human cells. Our experiments revealed that yeast cells primarily rely on the cytosolic ubiquitin-proteasome system, while human cells depend more on mitochondrial factors. Our findings suggest that understanding these mechanisms could provide insights into human diseases related to protein misfolding.