Modulation of autophagy by RTN-1C: role in autophagosome biogenesis

Manuela D’ Eletto, Anna Risuglia, Serafina Oliverio, Bisan Mehdawy, Roberta Nardacci, Matteo Bordi, Federica Di Sano

Research output: Contribution to journalArticlepeer-review


The endoplasmic reticulum (ER) is a key organelle fundamental for the maintenance of cellular homeostasis and to determine the cell’s fate under stress conditions. Among the known proteins that regulate ER structure and function there is Reticulon-1C (RTN-1C), a member of the reticulon family localized primarily on the ER membrane. We previously demonstrated that RTN-1C expression affects ER function and stress condition. ER is an essential site for the regulation of apoptotic pathways and it has also been recently recognized as an important component of autophagic signaling. Based on these evidences, we have investigated the impact of RTN-1C modulation on autophagy induction. Interestingly we found that reticulon overexpression is able to activate autophagic machinery and its silencing results in a significative inhibition of both basal and induced autophagic response. Using different experimental approaches we demonstrated that RTN-1C colocalizes with ATG16L and LC3II on the autophagosomes. Considering the key role of reticulon proteins in the control of ER membrane shaping and homeostasis, our data suggest the participation of RTN-1C in the autophagic vesicle biogenesis at the level of the ER compartment. Our data indicate a new mechanism by which this structural ER protein modulates cellular stress, that is at the basis of different autophagy-related pathologies.

Original languageEnglish
Article number868
Pages (from-to)1-14
Number of pages14
JournalCell Death and Disease
Issue number12
Publication statusPublished - Dec 1 2019

ASJC Scopus subject areas

  • Immunology
  • Cellular and Molecular Neuroscience
  • Cell Biology
  • Cancer Research


Dive into the research topics of 'Modulation of autophagy by RTN-1C: role in autophagosome biogenesis'. Together they form a unique fingerprint.

Cite this