IFNB/interferon-β regulates autophagy via a MIR1-TBC1D15-RAB7 pathway

Patrick Ejlerskov, David C. Rubinsztein, Roger Pocock

Research output: Contribution to journalEditorialOtherpeer-review

Abstract

Loss of IFNB/interferon-β in mice causes a Parkinson disease-like phenotype where many features, including SNCA/α-synuclein and MAPT/tau accumulation, can be attributed to a late-stage block in autophagic flux. Recently, we identified a mechanism that can explain this phenotype. We found that IFNB induces expression of Mir1, a microRNA that can reduce the levels of TBC1D15, a RAB GTPase-activating protein. Induction of this pathway decreases RAB7 activity and thereby stimulates macroautophagy/autophagy. The relevance of these key players is deeply conserved from humans to Caenorhabditis elegans, highlighting the importance of this ancient autophagy regulatory pathway.

Original languageEnglish
Pages (from-to)767-769
Number of pages3
JournalAutophagy
Volume16
Issue number4
DOIs
Publication statusPublished - 2020

Keywords

  • Autophagy
  • Huntington disease
  • interferon-beta
  • miR-1
  • Parkinson disease
  • proteinopathies
  • TBC1D15

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