IFNB/interferon-β regulates autophagy via a MIR1-TBC1D15-RAB7 pathway. Issue 4 (2nd April 2020)

• Record Type: Journal Article
• Authors: Ejlerskov, Patrick; Rubinsztein, David C.; Pocock, Roger
• Is Part Of: Autophagy. Volume 16:Issue 4(2020)
• Page Start: 767
• Page End: 769
• Publication Date: 2020-04-02
• Subjects: Autophagy -- Huntington disease -- interferon-beta -- miR-1 -- Parkinson disease -- proteinopathies -- TBC1D15; Autophagic vacuoles -- Periodicals; Apoptosis -- Periodicals; Cell death -- Periodicals; Lysosomes -- Periodicals; Degeneration (Pathology) -- Periodicals; Autophagy -- Periodicals; Cell Death -- Periodicals; Lysosomes -- Periodicals; Periodicals; 571.936
• DOI: 10.1080/15548627.2020.1718384
• Languages: English
• ISSNs: 1554-8627

Abstract

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.