Polo-like Kinase 1 (PLK1) Regulates Interferon (IFN) Induction by MAVS

Vitour, Damien; Dabo, StÃ©phanie; Pour, Malek Ahmadi; Vilasco, Myriam; Vidalain, Pierre‐Olivier; Jacob, Yves; Mezel-Lemoine, Mariana; Paz, Suzanne; Arguello, Meztli; Lin, Rongtuan; Tangy, FrÃ©dÃ©ric; Hiscott, John; Meurs, Éliane

doi:10.1074/jbc.m109.018275

Cited by 85 publications

(68 citation statements)

References 57 publications

(42 reference statements)

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“…Indeed, Plk1 has been shown to interact with the mitochondria-bound adaptor MAVS and to inhibit the ability of MAVS to activate the IRF3 and NFκB pathway. 84 Another intriguing issue concerns the importance of these phosphorylation events in post-Golgi membrane trafficking.…”

Section: Subcellular Localization Of Optnmentioning

confidence: 99%

Toward an integrative view of Optineurin functions

et al. 2012

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Section: Subcellular Localization Of Optnmentioning

confidence: 99%

Toward an integrative view of Optineurin functions

et al. 2012

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“…The pUC19 plasmid was from Invitrogen. The pEF-BOS FLAG-RIG-I plasmid was described previously (62,66). Full-length MDA5, cloned into the pDON207R (Invitrogen) construct provided by P.-O.…”

Section: Rna Extraction and Real-time Quantitative Reverse Transcriptmentioning

confidence: 99%

Sensing and Control of Bluetongue Virus Infection in Epithelial Cells via RIG-I and MDA5 Helicases

Chauveau

Doceul

Lara

et al. 2012

J Virol

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Bluetongue virus (BTV), an arthropod-borne member of the Reoviridae family, is a double-stranded RNA virus that causes an economically important livestock disease that has spread across Europe in recent decades. Production of type I interferon (alpha/beta interferon [IFN-␣/␤]) has been reported in vivo and in vitro upon BTV infection. However, the cellular sensors and signaling pathways involved in this process remain unknown. Here we studied the mechanisms responsible for the production of IFN-␤ in response to BTV serotype 8. Upon BTV infection of A549 cells, expression of IFN-␤ and other proinflammatory cytokines was strongly induced at both the protein and mRNA levels. This response appeared to be dependent on virus replication, since exposure to UV-inactivated virus failed to induce IFN-␤. We also demonstrated that BTV infection activated the transcription factors IFN regulatory factor 3 and nuclear factor B. We investigated the role of several pattern recognition receptors in this response and showed that expression of IFN-␤ was greatly reduced after small-interfering-RNA-mediated knockdown of the RNA helicase encoded by retinoic acid-inducible gene I (RIG-I) or melanoma differentiation-associated gene 5 (MDA5). In contrast, silencing of MyD88, Toll-like receptor 3, or the recently described DexD/H-box helicase DDX1 sensor had no or a weak effect on IFN-␤ induction, suggesting that the RIG-I-like receptor pathway is specifically engaged for BTV sensing. Moreover, we also showed that overexpression of either RIG-I or MDA5 impaired BTV expression in infected A549 cells. Overall, this indicates that RIG-I and MDA5 can both contribute to the recognition and control of BTV infection.

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“…As a control, we expressed the Polo-like kinase 1 Polo-box domain (Plk1-PBD), an antagonist of the RLR pathway (36). As shown in Fig.…”

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confidence: 99%