AI Article Synopsis
- TRAF6 is crucial for activating TBK1/IKKε, which leads to type I interferon production and antiviral immune responses.
- Prmt2, an arginine methyltransferase in zebrafish, negatively regulates TRAF6 by dimethylating it, hindering its function and K63-linked polyubiquitination.
- This study shows that reducing prmt2 enhances the survival of zebrafish larvae exposed to a viral infection, highlighting a new role for prmt2 in dampening antiviral responses.
Article Abstract
TNFR-associated factor 6 (TRAF6) not only recruits TBK1/IKKε to MAVS upon virus infection but also catalyzes K63-linked polyubiquitination on substrate or itself, which is critical for NEMO-dependent and -independent TBK1/IKKε activation, leading to the production of type I IFNs. The regulation at the TRAF6 level could affect the activation of antiviral innate immunity. In this study, we demonstrate that zebrafish , a type I arginine methyltransferase, attenuates traf6-mediated antiviral response. Prmt2 binds to the C terminus of traf6 to catalyze arginine asymmetric dimethylation of traf6 at arginine 100, preventing its K63-linked autoubiquitination, which results in the suppression of traf6 activation. In addition, it seems that the N terminus of prmt2 competes with mavs for traf6 binding and prevents the recruitment of tbk1/ikkε to mavs. By zebrafish model, we show that loss of promotes the survival ratio of zebrafish larvae after challenge with spring viremia of carp virus. Therefore, we reveal, to our knowledge, a novel function of prmt2 in the negative regulation of antiviral innate immunity by targeting traf6.
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| http://dx.doi.org/10.4049/jimmunol.2100627 | DOI Listing |
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