Journal
CELL REPORTS
Volume 20, Issue 12, Pages 2944-2954Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.08.085
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Funding
- Japan Society for the Promotion of Science KAKENHI [26713005, 23659231, 26111501, 16H01189]
- Ministry of Education, Culture, Sports, Science, and Technology KAKENHI [17H06009, 17H06415]
- Takeda Science Foundation
- Japan Foundation for Pediatric Research
- NIH [PO1-AI070167]
- Grants-in-Aid for Scientific Research [26713005, 23659231, 17H06009, 16H01189, 17H06415, 15K07039, 17H06413, 17H05682, 26111501] Funding Source: KAKEN
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Cyclic GMP-AMP synthase (cGAS) is a cytosolic DNA sensor that induces the IFN antiviral response. However, the regulatory mechanisms thatmediate cGAS-triggered signaling have not been fully explored. Here, we show the involvement of a small GTPase, RAB2B, and its effector protein, Golgi-associated RAB2B interactor-like 5 (GARIL5), in the cGAS-mediated IFN response. RAB2B-deficiency affects the IFN response induced by cytosolic DNA. Consistent with this, RAB2B deficiency enhances replication of vaccinia virus, a DNA virus. After DNA stimulation, RAB2B colocalizes with stimulator of interferon genes (STING), the downstream signal mediator of cGAS, on the Golgi apparatus. The GTP-binding activity of RAB2B is required for its localization on the Golgi apparatus and for recruitment of GARIL5. GARIL5 deficiency also affects the IFN response induced by cytosolic DNA and enhances replication of vaccinia virus. These findings indicate that the RAB2B-GARIL5 complex promotes IFN responses against DNA viruses by regulating the cGAS-STING signaling axis.
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