Specific association of TBK1 with the trans-Golgi network following STING stimulation

Stimulator of interferon genes (STING) is essential for the type I interferon response induced by microbial DNA or self-DNA leaked from mitochondria/nuclei. In response to the emergence of such DNAs in the cytosol, STING relocates from the endoplasmic reticulum (ER) to the Golgi, and activates TANK-...

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Published inCell Structure and Function Vol. 47; no. 1; pp. 19 - 30
Main Authors Kemmoku, Haruka, Kuchitsu, Yoshihiko, Mukai, Kojiro, Taguchi, Tomohiko
Format Journal Article
LanguageEnglish
Published Japan Japan Society for Cell Biology 01.01.2022
Japan Science and Technology Agency
Subjects
CRISPR
Cytosol
Endoplasmic Reticulum
Golgi Apparatus
Humans
Immunity, Innate
Inflammatory diseases
innate immunity
Interferon
Kinases
Membrane Proteins - genetics
membrane traffic
Mitochondrial DNA
Protein Serine-Threonine Kinases - genetics
Proteins
Signal Transduction
STING
the Golgi
trans-Golgi Network
Vascular diseases
STING
innate immunity
membrane traffic
the Golgi
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Summary:Stimulator of interferon genes (STING) is essential for the type I interferon response induced by microbial DNA or self-DNA leaked from mitochondria/nuclei. In response to the emergence of such DNAs in the cytosol, STING relocates from the endoplasmic reticulum (ER) to the Golgi, and activates TANK-binding kinase 1 (TBK1), a cytosolic kinase essential for the activation of STING-dependent downstream signalling. To understand at which subcellular compartments TBK1 becomes associated with STING, we generated cells stably expressing fluorescent protein-tagged STING (mNeonGreen-STING) and TBK1 (TBK1-mScarletI). We found that after STING stimulation, TBK1 became associated with the trans-Golgi network (TGN), not the other parts of the Golgi. STING variants that constitutively induce the type I interferon response have been identified in patients with autoinflammatory diseases named “STING-associated vasculopathy with onset in infancy (SAVI)”. Even in cells expressing these constitutively active STING variants, TBK1 was found to be associated with TGN, not the other parts of the Golgi. These results suggest that TGN acts as a specific platform where STING associates with and activates TBK1.Key words: the Golgi, membrane traffic, innate immunity, STING
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0386-7196
1347-3700
DOI:10.1247/csf.21080