FAS-associated factor-1 positively regulates type I interferon response to RNA virus infection by targeting NLRX1

FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-κB activity, ubiquitination, and proteasomal degradation. Here, we found that FAF1 positively regulates the type I interferon pathway. FAF1gt/gt mice, which defic...

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Published inPLoS pathogens Vol. 13; no. 5; p. e1006398
Main Authors Kim, Jae-Hoon, Park, Min-Eun, Nikapitiya, Chamilani, Kim, Tae-Hwan, Uddin, Md Bashir, Lee, Hyun-Cheol, Kim, Eunhee, Ma, Jin Yeul, Jung, Jae U., Kim, Chul-Joong, Lee, Jong-Soo
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 01.05.2017
Public Library of Science (PLoS)
Subjects
Adaptor Proteins, Signal Transducing - genetics
Adaptor Proteins, Signal Transducing - immunology
Animals
Apoptosis
Apoptosis Regulatory Proteins
Biology and Life Sciences
Carrier Proteins - genetics
Carrier Proteins - immunology
Cellular signal transduction
Cytokines
Death
Degradation
Development and progression
Fas antigen
Female
Genetic aspects
Humans
Immune system
Infections
Inflammation
Interferon
Interferon Type I - genetics
Interferon Type I - immunology
Intracellular Signaling Peptides and Proteins
Kinases
Macrophages - immunology
Macrophages - virology
Male
Medicine and Health Sciences
Mice
Mice, Inbred C57BL
Mice, Knockout
Mitochondrial Proteins - genetics
Mitochondrial Proteins - immunology
Mortality
NF-kappa B - genetics
NF-kappa B - immunology
NF-κB protein
Physiological aspects
Proteasomes
Research and Analysis Methods
Ribonucleic acid
RNA
RNA virus infections
RNA Virus Infections - genetics
RNA Virus Infections - immunology
RNA Virus Infections - virology
RNA viruses
RNA Viruses - physiology
Ubiquitination
Veterinary colleges
Viruses
Bangladesh
South Korea
Online AccessGet full text
ISSN1553-7374
1553-7366
1553-7374
DOI10.1371/journal.ppat.1006398

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Abstract FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-κB activity, ubiquitination, and proteasomal degradation. Here, we found that FAF1 positively regulates the type I interferon pathway. FAF1gt/gt mice, which deficient in FAF1, and FAF1 knockdown immune cells were highly susceptible to RNA virus infection and showed low levels of inflammatory cytokines and type I interferon (IFN) production. FAF1 was bound competitively to NLRX1 and positively regulated type I IFN signaling by interfering with the interaction between NLRX1 and MAVS, thereby freeing MAVS to bind RIG-I, which switched on the MAVS-RIG-I-mediated antiviral signaling cascade. These results highlight a critical role of FAF1 in antiviral responses against RNA virus infection.
AbstractList FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-κB activity, ubiquitination, and proteasomal degradation. Here, we found that FAF1 positively regulates the type I interferon pathway. FAF1gt/gt mice, which deficient in FAF1, and FAF1 knockdown immune cells were highly susceptible to RNA virus infection and showed low levels of inflammatory cytokines and type I interferon (IFN) production. FAF1 was bound competitively to NLRX1 and positively regulated type I IFN signaling by interfering with the interaction between NLRX1 and MAVS, thereby freeing MAVS to bind RIG-I, which switched on the MAVS-RIG-I-mediated antiviral signaling cascade. These results highlight a critical role of FAF1 in antiviral responses against RNA virus infection.FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-κB activity, ubiquitination, and proteasomal degradation. Here, we found that FAF1 positively regulates the type I interferon pathway. FAF1gt/gt mice, which deficient in FAF1, and FAF1 knockdown immune cells were highly susceptible to RNA virus infection and showed low levels of inflammatory cytokines and type I interferon (IFN) production. FAF1 was bound competitively to NLRX1 and positively regulated type I IFN signaling by interfering with the interaction between NLRX1 and MAVS, thereby freeing MAVS to bind RIG-I, which switched on the MAVS-RIG-I-mediated antiviral signaling cascade. These results highlight a critical role of FAF1 in antiviral responses against RNA virus infection.
FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-κB activity, ubiquitination, and proteasomal degradation. Here, we found that FAF1 positively regulates the type I interferon pathway. FAF1gt/gt mice, which deficient in FAF1, and FAF1 knockdown immune cells were highly susceptible to RNA virus infection and showed low levels of inflammatory cytokines and type I interferon (IFN) production. FAF1 was bound competitively to NLRX1 and positively regulated type I IFN signaling by interfering with the interaction between NLRX1 and MAVS, thereby freeing MAVS to bind RIG-I, which switched on the MAVS-RIG-I-mediated antiviral signaling cascade. These results highlight a critical role of FAF1 in antiviral responses against RNA virus infection.
FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-KB activity, ubiquitination, and proteasomal degradation. Here, we found that FAF1 positively regulates the type I interferon pathway. FAF1gt/gt mice, which deficient in FAF1, and FAF1 knockdown immune cells were highly susceptible to RNA virus infection and showed low levels of inflammatory cytokines and type I interferon (IFN) production. FAF1 was bound competitively to NLRX1 and positively regulated type I IFN signaling by interfering with the interaction between NLRX1 and MAVS, thereby freeing MAVS to bind RIG-I, which switched on the MAVS-RIG-I-mediated antiviral signaling cascade. These results highlight a critical role of FAF1 in antiviral responses against RNA virus infection.
FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-κB activity, ubiquitination, and proteasomal degradation. Here, we found that FAF1 positively regulates the type I interferon pathway. FAF1 gt/gt mice, which deficient in FAF1, and FAF1 knockdown immune cells were highly susceptible to RNA virus infection and showed low levels of inflammatory cytokines and type I interferon (IFN) production. FAF1 was bound competitively to NLRX1 and positively regulated type I IFN signaling by interfering with the interaction between NLRX1 and MAVS, thereby freeing MAVS to bind RIG-I, which switched on the MAVS-RIG-I-mediated antiviral signaling cascade. These results highlight a critical role of FAF1 in antiviral responses against RNA virus infection. Type I interferon-mediated antiviral response is critical for controlling virus infections. However, interferon-mediated immune responses need to be tightly regulated to maintain host immune homeostasis. Recently, molecules involved in regulating interferon-mediated innate immune response are the subject of much research. Among these, the first protein to be identified as a negative regulator of MAVS was the nucleotide-binding domain and leucine-rich repeat containing family member, NLRX1. NLRX1 associates with MAVS to inhibit antiviral signaling by interrupting virus-induced RLR-MAVS interactions. Interestingly, we found that FAF1 interacts with NLRX1 in response to RNA virus infection and this interaction inhibits binding of MAVS to NLRX1, which in turn switches on RIG-I mediated antiviral immune responses. As results, we showed that FAF1 gt/gt mice, which deficient in FAF1, and FAF1 knockdown immune cells were highly susceptible to RNA virus infection and showed low levels of inflammatory cytokines and type I interferon (IFN) production. Our findings suggest that FAF1 is a crucial regulator that induces the antiviral innate immune responses against RNA virus infection.
FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-[kappa]B activity, ubiquitination, and proteasomal degradation. Here, we found that FAF1 positively regulates the type I interferon pathway. FAF1.sup.gt/gt mice, which deficient in FAF1, and FAF1 knockdown immune cells were highly susceptible to RNA virus infection and showed low levels of inflammatory cytokines and type I interferon (IFN) production. FAF1 was bound competitively to NLRX1 and positively regulated type I IFN signaling by interfering with the interaction between NLRX1 and MAVS, thereby freeing MAVS to bind RIG-I, which switched on the MAVS-RIG-I-mediated antiviral signaling cascade. These results highlight a critical role of FAF1 in antiviral responses against RNA virus infection.
Audience Academic
Author Lee, Jong-Soo
Park, Min-Eun
Kim, Tae-Hwan
Ma, Jin Yeul
Nikapitiya, Chamilani
Lee, Hyun-Cheol
Kim, Chul-Joong
Uddin, Md Bashir
Kim, Eunhee
Kim, Jae-Hoon
Jung, Jae U.
AuthorAffiliation 1 College of Veterinary Medicine, Chungnam National University, Daejeon, Republic of Korea
3 College of Biological Sciences and Biotechnology, Chungnam National University, Daejeon, Korea
4 Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM), Daegu, Republic of Korea
University of North Carolina at Chapel Hill, UNITED STATES
2 Faculty of Veterinary & Animal Science, Sylhet Agricultural University, Sylhet, Bangladesh
5 Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, California, United States of America
AuthorAffiliation_xml – name: 1 College of Veterinary Medicine, Chungnam National University, Daejeon, Republic of Korea
– name: 2 Faculty of Veterinary & Animal Science, Sylhet Agricultural University, Sylhet, Bangladesh
– name: University of North Carolina at Chapel Hill, UNITED STATES
– name: 4 Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM), Daegu, Republic of Korea
– name: 5 Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, California, United States of America
– name: 3 College of Biological Sciences and Biotechnology, Chungnam National University, Daejeon, Korea
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  orcidid: 0000-0001-5119-0711
  surname: Lee
  fullname: Lee, Jong-Soo
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28542569$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright COPYRIGHT 2017 Public Library of Science
2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Kim J-H, Park M-E, Nikapitiya C, Kim T-H, Uddin MB, Lee H-C, et al. (2017) FAS-associated factor-1 positively regulates type I interferon response to RNA virus infection by targeting NLRX1. PLoS Pathog 13(5): e1006398. https://doi.org/10.1371/journal.ppat.1006398
2017 Kim et al 2017 Kim et al
2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Kim J-H, Park M-E, Nikapitiya C, Kim T-H, Uddin MB, Lee H-C, et al. (2017) FAS-associated factor-1 positively regulates type I interferon response to RNA virus infection by targeting NLRX1. PLoS Pathog 13(5): e1006398. https://doi.org/10.1371/journal.ppat.1006398
Copyright_xml – notice: COPYRIGHT 2017 Public Library of Science
– notice: 2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Kim J-H, Park M-E, Nikapitiya C, Kim T-H, Uddin MB, Lee H-C, et al. (2017) FAS-associated factor-1 positively regulates type I interferon response to RNA virus infection by targeting NLRX1. PLoS Pathog 13(5): e1006398. https://doi.org/10.1371/journal.ppat.1006398
– notice: 2017 Kim et al 2017 Kim et al
– notice: 2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Kim J-H, Park M-E, Nikapitiya C, Kim T-H, Uddin MB, Lee H-C, et al. (2017) FAS-associated factor-1 positively regulates type I interferon response to RNA virus infection by targeting NLRX1. PLoS Pathog 13(5): e1006398. https://doi.org/10.1371/journal.ppat.1006398
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Conceptualization: JSL.Formal analysis: JHK MEP.Investigation: JHK MEP CN MBU.Methodology: JHK MEP THK HCL.Project administration: JHK MEP.Resources: EK JYM JUJ CJK.Supervision: JSL.Writing – original draft: JHK JSL.
The authors have declared that no competing interests exist.
ORCID 0000-0002-0045-9669
0000-0002-7738-1222
0000-0001-8796-0394
0000-0001-5119-0711
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SSID ssj0041316
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Snippet FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-κB activity,...
FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-[kappa]B activity,...
FAS-associated factor-1 (FAF1) is a component of the death-inducing signaling complex involved in Fas-mediated apoptosis. It regulates NF-KB activity,...
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SubjectTerms Adaptor Proteins, Signal Transducing - genetics
Adaptor Proteins, Signal Transducing - immunology
Animals
Apoptosis
Apoptosis Regulatory Proteins
Biology and Life Sciences
Carrier Proteins - genetics
Carrier Proteins - immunology
Cellular signal transduction
Cytokines
Death
Degradation
Development and progression
Fas antigen
Female
Genetic aspects
Humans
Immune system
Infections
Inflammation
Interferon
Interferon Type I - genetics
Interferon Type I - immunology
Intracellular Signaling Peptides and Proteins
Kinases
Macrophages - immunology
Macrophages - virology
Male
Medicine and Health Sciences
Mice
Mice, Inbred C57BL
Mice, Knockout
Mitochondrial Proteins - genetics
Mitochondrial Proteins - immunology
Mortality
NF-kappa B - genetics
NF-kappa B - immunology
NF-κB protein
Physiological aspects
Proteasomes
Research and Analysis Methods
Ribonucleic acid
RNA
RNA virus infections
RNA Virus Infections - genetics
RNA Virus Infections - immunology
RNA Virus Infections - virology
RNA viruses
RNA Viruses - physiology
Ubiquitination
Veterinary colleges
Viruses
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  providerName: ProQuest
Title FAS-associated factor-1 positively regulates type I interferon response to RNA virus infection by targeting NLRX1
URI https://www.ncbi.nlm.nih.gov/pubmed/28542569
https://www.proquest.com/docview/1910461575
https://www.proquest.com/docview/1903161239
https://pubmed.ncbi.nlm.nih.gov/PMC5456407
https://doaj.org/article/d4a46eddce93432794a347fa637a2378
http://dx.doi.org/10.1371/journal.ppat.1006398
Volume 13
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