Abstract
Increasing evidence suggests important roles for long noncoding RNAs (lncRNAs) as new gene modulators involved in various biological processes. However, the function roles of lncRNAs in lower vertebrates are still unknown. Here, we firstly identify a lncRNA, named MAVS antiviral-related lncRNA (MARL), as a key regulator for antiviral immunity in teleost fish. The results indicate that fish MAVS play essential roles in host antiviral responses and inhibition of Siniperca chuatsi rhabdovirus (SCRV) replication. miR-122 reduces MAVS expression and suppress MAVS-mediated antiviral responses, which may help viruses evade host antiviral responses. Further, MARL functions as a competing endogenous RNA (ceRNA) for miR-122 to control protein abundance of MAVS, thereby inhibiting SCRV replication and promoting antiviral responses. Our data not only shed new light on understanding the function role of lncRNA in biological processes in lower vertebrates, but confirmed the hypothesis that ceRNA regulatory networks exist widely in vertebrates.
Highlights
Viral infection triggers host immune responses to rapidly detect and eliminate invading viruses, thereby survival of the host
Increasing evidence indicates that long noncoding RNAs (lncRNAs) participate in the regulation of various biological processes, especially innate and adaptive immunity
Our results provided the first direct evidence that a lncRNA, termed mitochondrial antiviral signaling protein (MAVS) antiviral-related lncRNA (MARL), acts as a key regulator for antiviral immunity in lower vertebrates. lncRNAs have been identified to function as competing endogenous RNAs and cross-talk with mRNAs by competing shared for miRNAs
Summary
Viral infection triggers host immune responses to rapidly detect and eliminate invading viruses, thereby survival of the host. Detection of viral infection involves Toll-like receptors (TLRs) and retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) that initiate signaling cascades to coordinately lead to the production of type-I interferons (IFNs) [1, 2]. Unlike the TLR receptors mediating antiviral responses, RLRs receptors RIG-I and MDA5 function as cytoplasmic sensors for viral RNA recognition [3]. Both RIG-I and MDA5 contain a C-terminal DExD/H box RNA helicase domain that directly interacts with viral RNAs and two N-terminal caspase activation and recruitment domains (CARDs) that promote the CARD-mediated downstream signaling cascade to activate the essential adaptor mitochondrial antiviral signaling protein (MAVS; termed IPS-1/Cardif/VISA) [3,4,5]. The regulation mechanisms of MAVS-mediated signaling need be extensively investigated
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