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.

中文翻译：

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IFNB/干扰素-β通过 MIR1-TBC1D15-RAB7 通路调节自噬。

小鼠中 IFNB/干扰素-β 的缺失导致帕金森病样表型，其中许多特征，包括 SNCA/α-突触核蛋白和 MAPT/tau 积累，可归因于自噬通量的晚期阻滞。最近，我们发现了一种可以解释这种表型的机制。我们发现 IFNB 诱导 Mir1 的表达，这是一种可以降低 RAB GTPase 激活蛋白 TBC1D15 水平的 microRNA。该通路的诱导降低了 RAB7 的活性，从而刺激了巨自噬/自噬。这些关键参与者的相关性从人类到秀丽隐杆线虫都得到了深刻的保护，突出了这种古老的自噬调节途径的重要性。