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The long noncoding RNA Lnczc3h7a promotes TRIM25-mediated RIG-I antiviral innate immune response

ABSTRACT: In this study, we employed a combination of RIP-seq and iCLIP-seq technologies to identify long non-coding RNA associated with cytoplasmic TRIM25 and RIG-I protein in mouse macrophages cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE112175 | GEO | 2019/03/12

REPOSITORIES: GEO

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Self-recognition of an inducible host lncRNA by RIG-I feedback restricts innate immune response

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The long noncoding RNA Lnczc3h7a promotes TRIM25-mediated RIG-I antiviral innate immune response

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Project description:The RIG-I-like receptors (RLRs: RIG-I, MDA5 and LGP2) trigger inflammatory and antiviral responses by sensing non-self RNA molecules produced during viral replication. LGP2 regulation of RIG-I and MDA5-dependant type-I interferon signaling is a matter of controversy. Here we show that LGP2 interacts with different components of the RNA silencing machinery. Particularly, we identified a direct protein-protein interaction between LGP2 and interferon-inducible double-stranded RNA-dependent protein kinase activator A (PACT). The LGP2-PACT interaction is mediated by the regulatory C-terminal domain of LGP2 and is necessary for inhibiting the RIG-I- and amplifying the MDA5-responses. We describe a point mutation within LGP2 that disrupts LGP2-PACT interaction and leads to the loss of LGP2 regulatory activity over RIG-I and MDA5. These results provide a model in which PACT-LGP2 interaction regulates RIG-I and MDA5 inflammatory response and allows cellular RNA silencing machinery to coordinate the innate immune response.

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2020-09-17 | GSE158122 | GEO

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