Journal
NATURE COMMUNICATIONS
Volume 5, Issue -, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/ncomms5713
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Funding
- JSPS KAKENHI [25115515, 26291032, 26620135]
- Kyushu University Interdisciplinary Programs in Education and Projects in Research Development
- Uehara Memorial Foundation
- Takeda Science Foundation
- Kao Foundation for Arts and Sciences
- Tokyo Biochemical Research Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Sasakawa Scientific Research Grant from the Japan Science Society
- Joint Research Project of the Institute of Medical Science, the University of Tokyo
- Grants-in-Aid for Scientific Research [25713018, 25115515, 26291032, 26620135, 25440088] Funding Source: KAKEN
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Mitochondria contribute to cellular innate immunity against RNA viruses. Mitochondrial-mediated innate immunity is regulated by signalling molecules that are recruited to the mitochondrial membrane, and depends on the mitochondrial inner membrane potential (Delta psi(m)). Here we examine the physiological relevance of Delta psi(m) and the mitochondrial-associating influenza A viral protein PB1-F2 in innate immunity. When expressed in host cells, PB1-F2 completely translocates into the mitochondrial inner membrane space via Tom40 channels, and its accumulation accelerates mitochondrial fragmentation due to reduced Delta psi(m). By contrast, PB1-F2 variants lacking a C-terminal polypeptide, which is frequently found in low pathogenic subtypes, do not affect mitochondrial function. PB1-F2-mediated attenuation of Delta psi(m) suppresses the RIG-I signalling pathway and activation of NLRP3 inflammasomes. PB1-F2 translocation into mitochondria strongly correlates with impaired cellular innate immunity, making this translocation event a potential therapeutic target.
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