You are here: Home / Research / Upcoming Seminars / Paolo Grumati, MD, Ph.D. - "How autophagy regulates endoplasmic reticulum turnover"

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
Add event to calendar vCal

Short CV

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.

Filed under: