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Paolo Grumati, MD, Ph.D. - "How autophagy regulates endoplasmic reticulum turnover"

Institute of Biochemistry II, Goethe University School of Medicine, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany
When Sep 19, 2017
from 12:00 PM to 01:30 PM
Where Tigem Auditorium "Vesuvius"
Contact Name
Contact Phone 08119230649
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Abstract
The turnover of endoplasmic reticulum (ER) ensures the correct biological activity of all its distinct domains. In mammalian cells the ER is degraded via selective autophagy pathway (ER-phagy) mediated by two specific receptors: FAM134B, responsible for ER sheets turnover and SEC62 that regulates ER recovery after stress. We identified reticulon 3 (RTN3) as a specific receptor for degradation of the ER tubules. Oligomerization of the long isoform of RTN3 is sufficient to trigger tubular ER fragmentation. The long N-terminal region of RTN3 contains several newly identified LC3-interacting regions (LIR). The binding to LC3/GABARAPs is essential for the fragmentation of ER tubules and their delivery to lysosomes. RTN3-mediated ER-phagy requires conventional autophagy components, but is independent from FAM134B. None of the other reticulon members has the ability to induce fragmentation of ER tubules during starvation. Therefore, we assign a unique function to RTN3 during autophagy of ER tubules.

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