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LGP2 virus sensor enhances apoptosis by upregulating apoptosis-regulatory genes through TRBP-bound miRNAs during viral infection

ABSTRACT: LGP2 virus sensor enhances apoptosis by upregulating apoptosis-regulatory genes through TRBP-bound miRNAs during viral infection

PROVIDER: PRJNA559265 | ENA |

REPOSITORIES: ENA

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LGP2 virus sensor enhances apoptosis by upregulating apoptosis-regulatory genes through TRBP-bound miRNAs during viral infection

Project description:To reveal the fuction of cytoplasmic virus sensor protein, LGP2, on RNA silencing, we analyzed gene expression profiles on HeLa WT and LGP2 knockout cells during SeV infection, which were generated with CRISPR/Cas system.

2019-11-20 | GSE135547 | GEO

Caspase-mediated processing of TRBP regulates apoptosis during viral infection

Project description:RNA silencing is a post-transcriptional gene-silencing mechanism mediated by microRNAs (miRNAs). However, the regulatory mechanism of RNA silencing during viral infection is unclear. TAR RNA-binding protein (TRBP) is an enhancer of RNA silencing that induces miRNA maturation by interacting with the ribonuclease Dicer. TRBP interacts with a virus sensor protein, laboratory of genetics and physiology 2 (LGP2), in the early stage of viral infection of human cells. Next, it induces apoptosis by inhibiting the maturation of miRNAs, thereby upregulating the expression of apoptosis regulatory genes. In this study, we show that TRBP undergoes a functional conversion in the late stage of viral infection. Viral infection resulted in the activation of caspases that proteolytically processed TRBP into two fragments. The N-terminal fragment did not interact with Dicer but interacted with type I interferon (IFN) signaling modulators, such as protein kinase R (PKR) and LGP2, and induced ER stress. The end results were irreversible apoptosis and suppression of IFN signaling. Our results demonstrate that the processing of TRBP enhances apoptosis, reducing IFN signaling during viral infection.

2024-04-19 | GSE234549 | GEO

Caspase-mediated processing of TRBP regulates apoptosis during viral infection

2024-04-19 | GSE234547 | GEO

LGP2 virus sensor regulates gene expression network mediated by TRBP-bound microRNAs.

2018-06-29 | GSE113028 | GEO

LGP2 virus sensor regulates gene expression network mediated by TRBP-bound microRNAs.

Project description:LGP2 virus sensor regulates gene expression network mediated by TRBP-bound microRNAs.

| PRJNA449826 | ENA

LGP2 virus sensor enhances apoptosis by upregulating apoptosis regulatory genes through TRBP-bound miRNAs during viral infection.

Project description:During viral infection, viral nucleic acids are detected by virus sensor proteins including toll-like receptor 3 or retinoic acid-inducible gene I-like receptors (RLRs) in mammalian cells. Activation of these virus sensor proteins induces type-I interferon production and represses viral replication. Recently, we reported that an RLR family member, laboratory of genetics and physiology 2 (LGP2), modulates RNA silencing by interacting with an RNA silencing enhancer, TAR-RNA binding protein (TRBP). However, the biological implications remained unclear. Here, we show that LGP2 enhances apoptosis by upregulating apoptosis regulatory genes during viral infection. Sendai virus (SeV) infection increased LGP2 expression approximately 900 times compared to that in non-virus-infected cells. Then, the induced LGP2 interacted with TRBP, resulting in the inhibition of maturation of the TRBP-bound microRNA (miRNA) and its subsequent RNA silencing activity. Gene expression profiling revealed that apoptosis regulatory genes were upregulated during SeV infection: caspases-2, -8, -3 and -7, four cysteine proteases with key roles in apoptosis, were upregulated directly or indirectly through the repression of a typical TRBP-bound miRNA, miR-106b. Our findings may shed light on the mechanism of apoptosis, induced by the TRBP-bound miRNAs through the interaction of TRBP with LGP2, as an antiviral defense system in mammalian cells.

| S-EPMC7026649 | biostudies-literature

Caspase-mediated processing of TRBP regulates apoptosis during viral infection

Project description:Caspase-mediated processing of TRBP regulates apoptosis during viral infection

| PRJNA982029 | ENA

Caspase-mediated processing of TRBP regulates apoptosis during viral infection

Project description:Caspase-mediated processing of TRBP regulates apoptosis during viral infection

| PRJNA982025 | ENA

Caspase-mediated processing of TRBP regulates apoptosis during viral infection

Project description:Caspase-mediated processing of TRBP regulates apoptosis during viral infection

| PRJNA982032 | ENA

LGP2 virus sensor regulates gene expression network mediated by TRBP-bound microRNAs.

Project description:Here we show that laboratory of genetics and physiology 2 (LGP2) virus sensor protein regulates gene expression network of endogenous genes mediated by TAR-RNA binding protein (TRBP)-bound microRNAs (miRNAs). TRBP is an enhancer of RNA silencing, and functions to recruit precursor-miRNAs (pre-miRNAs) to Dicer that processes pre-miRNA into mature miRNA. Viral infection activates the antiviral innate immune response in mammalian cells. Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), including RIG-I, melanoma-differentiation-associated gene 5 (MDA5), and LGP2, function as cytoplasmic virus sensor proteins during viral infection. RIG-I and MDA5 can distinguish between different types of RNA viruses to produce antiviral cytokines, including type I interferon. However, the role of LGP2 is controversial. We found that LGP2 bound to the double-stranded RNA binding sites of TRBP, resulting in inhibition of pre-miRNA binding and recruitment by TRBP. Furthermore, although it is unclear whether TRBP binds to specific pre-miRNA, we found that TRBP bound to particular pre-miRNAs with common structural characteristics. Thus, LGP2 represses specific miRNA activities by interacting with TRBP, resulting in selective regulation of target genes. Our findings show that a novel function of LGP2 is to modulate RNA silencing, indicating the crosstalk between RNA silencing and RLR signaling in mammalian cells.

| S-EPMC6158488 | biostudies-literature

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