Molecular cloning and functional analysis of the duck TIR domain-containing adaptor inducing IFN-β (TRIF) gene

Wei, Xiaojian; Qian, Wei; Sizhu, Suolang; Shi, Lijuan; Jin, Meilin

doi:10.1016/j.dci.2016.08.006

Cited by 5 publications

(8 citation statements)

References 41 publications

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“…To investigate whether duTRAF3 and duTRAF3-S are involved in duck type I IFN production pathway, DEFs were cotransfected with duTRAF3 or duTRAF3-S and a series of expression constructs encoding the molecules of RLRs signaling pathway or TLRs signaling pathway, including duRIG-I(N), duMDA5(N), duMAVS and duTRIF, or poly(I:C) (TLR3 agonist). Transfection of DEFs with duRIG-I(N), duMDA5(N), duTRIF, duMAVS, or poly(I:C) activated the IFN-β promoter activity, consistent with previous studies ( 22 , 33 – 35 ). Reporter assays showed that coexpression of duTRAF3 reproducibly enhanced the level of IFN-β promoter activity to constitutively activated cells expressing plasmids (Figure 3 A) as has been demonstrated in human TRAF3 ( 10 ).…”

Section: Resultssupporting

confidence: 90%

“…pCAGGS-HA expression plasmids encoding truncated duTRAF3 fragments, including HA-T31-216, HA-T321, HA-T3319, HA-Δcoil3, and HA-TRAF-C-domain, were obtained by PCR amplification of HA-duTRAF3. Based on the previous studies ( 22 – 25 ), duRIG-I, duRIG-I(N), duMDA5(N), duMAVS, and duTRIF were amplified from duck cDNA and cloned into the p3xFlag-CMV-14 vector with C -terminal Flag epitope tags. Flag-tagged duTLR3 was kindly provided by Dr. Peirong Jiao (Huanan Agricultural University).…”

Section: Methodsmentioning

confidence: 99%

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Negative Regulation of Interferon-β Production by Alternative Splicing of Tumor Necrosis Factor Receptor-Associated Factor 3 in Ducks

Wei

Qian

Sizhu³

et al. 2018

Front. Immunol.

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Tumor necrosis factor receptor-associated factor 3 (TRAF3), an intracellular signal transducer, is identified as an important component of Toll-like receptors and RIG-I-like receptors induced type I interferon (IFN) signaling pathways. Previous studies have clarified TRAF3 function in mammals, but little is known about the role of TRAF3 in ducks. Here, we cloned and characterized the full-length duck TRAF3 (duTRAF3) gene and an alternatively spliced isoform of duTRAF3 (duTRAF3-S) lacking the fragment encoding amino acids 217–319, from duck embryo fibroblasts (DEFs). We found that duTRAF3 and duTRAF3-S played different roles in regulating IFN-β production in DEFs. duTRAF3 through its TRAF domain interacted with duMAVS or duTRIF, leading to the production of IFN-β. However, duTRAF3-S, containing the TRAF domain, was unable to bind duMAVS or duTRIF due to the intramolecular binding between the N- and C-terminal of duTRAF3-S that blocked the function of its TRAF domain. Further analysis identified that duTRAF3-S competed with duTRAF3 itself for binding to duTRAF3, perturbing duTRAF3 self-association, which impaired the assembly of duTRAF3-duMAVS/duTRIF complex, ultimately resulted in a reduced production of IFN-β. These findings suggest that duTRAF3 is an important regulator of duck innate immune signaling and reveal a novel mechanism for the negative regulation of IFN-β production via changing the formation of the homo-oligomerization of wild molecules, implying a novel regulatory role of truncated proteins.

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Section: Resultssupporting

confidence: 90%

Section: Methodsmentioning

confidence: 99%

Negative Regulation of Interferon-β Production by Alternative Splicing of Tumor Necrosis Factor Receptor-Associated Factor 3 in Ducks

Wei

Qian

Sizhu³

et al. 2018

Front. Immunol.

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“…TRIF is the adaptor molecule downstream of TLR3 and TLR4 and provides a signaling platform to recruit other adaptor proteins and increase type I IFNs and proinflammatory cytokine expression (Figure 1). Similar to humans (Yamamoto et al, 2003), in uninfected tissues, ducks express TRIF most highly in the pancreas and spleen (Wei X. et al, 2016) (Figure 2B). Chicken TRIF expression was found to be highest in the cecum, heart, liver, spleen, and kidney (Wheaton et al, 2007).…”

Section: Trifmentioning

confidence: 60%

“…Chicken TRIF expression was found to be highest in the cecum, heart, liver, spleen, and kidney (Wheaton et al, 2007). Expression of duck TRIF peaks at 12 h after treatment with poly (I:C), however, it peaks much later at 36 h post infection with IAV (Wei X. et al, 2016), likely due to viral suppression of IFN signaling pathways in infected cells.…”

Section: Trifmentioning

confidence: 98%

Pattern Recognition Receptor Signaling and Innate Responses to Influenza A Viruses in the Mallard Duck, Compared to Humans and Chickens

Campbell

Magor

2020

Front. Cell. Infect. Microbiol.

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Mallard ducks are a natural host and reservoir of avian Influenza A viruses. While most influenza strains can replicate in mallards, the virus typically does not cause substantial disease in this host. Mallards are often resistant to disease caused by highly pathogenic avian influenza viruses, while the same strains can cause severe infection in humans, chickens, and even other species of ducks, resulting in systemic spread of the virus and even death. The differences in influenza detection and antiviral effectors responsible for limiting damage in the mallards are largely unknown. Domestic mallards have an early and robust innate response to infection that seems to limit replication and clear highly pathogenic strains. The regulation and timing of the response to influenza also seems to circumvent damage done by a prolonged or dysregulated immune response. Rapid initiation of innate immune responses depends on viral recognition by pattern recognition receptors (PRRs) expressed in tissues where the virus replicates. RIG-like receptors (RLRs), Toll-like receptors (TLRs), and Nod-like receptors (NLRs) are all important influenza sensors in mammals during infection. Ducks utilize many of the same PRRs to detect influenza, namely RIG-I, TLR7, and TLR3 and their downstream adaptors. Ducks also express many of the same signal transduction proteins including TBK1, TRIF, and TRAF3. Some antiviral effectors expressed downstream of these signaling pathways inhibit influenza replication in ducks. In this review, we summarize the recent advances in our understanding of influenza recognition and response through duck PRRs and their adaptors. We compare basal tissue expression and regulation of these signaling components in birds, to better understand what contributes to influenza resistance in the duck.

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“…Increasing intracellular signal transducers were identified, numerous studies showed that many proteins could be involved in DTMUV infection. For example, the TRIF in duck embryo fibroblasts (DEF) cells infected with DTMUV was upregulated [ 77 ], duck TRAF3 can interact with the upstream molecule TRIF, and leading to the production of IFN-β, overexpression of TRAF3 inhibited the replication of DTMUV [ 78 ], while the overexpression of duck TBK1 and IRF7 dramatically reduced the replication of DTMUV in DEF cells [ 79 – 81 ]. The results above clearly demonstrated that a TLR3-mediated signaling pathway was essential for defending against DTMUV infection.…”

Section: Dtmuv Infection Triggers Host Innate Immune Responsesmentioning

confidence: 99%

Innate immune responses to duck Tembusu virus infection

Zhao

Yang

et al. 2020

Vet Res

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The disease caused by duck Tembusu virus (DTMUV) is characterized by severe egg-drop in laying ducks. Currently, the disease has spread to most duck-raising areas in China, leading to great economic losses in the duck industry. In the recent years, DTMUV has raised some concerns, because of its expanding host range and increasing pathogenicity, as well as the potential threat to public health. Innate immunity is crucial for defending against invading pathogens in the early stages of infection. Recently, studies on the interaction between DTMUV and host innate immune response have made great progress. In the review, we provide an overview of DTMUV and summarize current advances in our understanding of the interaction between DTMUV and innate immunity, including the host innate immune responses to DTMUV infection through pattern recognition receptors (PRRs), signaling transducer molecules, interferon-stimulated genes (ISGs), and the immune evasion strategies employed by DTMUV. The aim of the review is to gain an in-depth understanding of DTMUV pathogenesis to facilitate future studies.

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Molecular cloning and functional analysis of the duck TIR domain-containing adaptor inducing IFN-β (TRIF) gene

Cited by 5 publications

References 41 publications

Negative Regulation of Interferon-β Production by Alternative Splicing of Tumor Necrosis Factor Receptor-Associated Factor 3 in Ducks

Negative Regulation of Interferon-β Production by Alternative Splicing of Tumor Necrosis Factor Receptor-Associated Factor 3 in Ducks

Pattern Recognition Receptor Signaling and Innate Responses to Influenza A Viruses in the Mallard Duck, Compared to Humans and Chickens

Innate immune responses to duck Tembusu virus infection

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