Bombyx mori lncRNA Unc-89-AS1 contributes to viral proliferation through modulating cell apoptosis.
TL;DR
Findings reveal a novel mechanism by which Lnc Unc-89-AS1 influences BmNPV infection by regulating apoptosis, providing new insights into host antiviral defenses relevant to the prevention and control of silkworm diseases.
Abstract
Long noncoding RNAs (lncRNAs) have been demonstrated to participate in apoptosis and host-virus interactions. Apoptosis is a host mechanism for defending against virus invasion. Bombyx mori nucleopolyhedrovirus (BmNPV) is one of the primary pathogens infecting the silkworm. However, little is known concerning whether the silkworm body activates apoptotic programs against BmNPV infection via lncRNAs. This study aimed to identify apoptosis-related lncRNAs involved in BmNPV infection in silkworms. Through transcriptome sequencing, the study identified a lncRNA co-expressed with BmIAP (Bombyx mori Inhibitor of Apoptosis Protein) named Lnc Unc-89-AS1. Fluorescence in situ hybridization (FISH) experiments indicated that Lnc Unc-89-AS1 was localized to both the nucleus and cytoplasm of BmE-SWU1 cells. We further investigated the regulatory role of Lnc Unc-89-AS1 in modulating apoptosis and BmNPV infection. Caspase activity assays, flow cytometry, qRT-PCR and mitochondrial membrane potential analysis demonstrated its function in inhibiting apoptosis in silkworm cells by participating in the mitochondrial apoptosis pathway. Overexpression and interference with Lnc Unc-89-AS1 in silkworm cells confirmed that it contributes to BmNPV proliferation at both the transcriptional and translational levels. These findings reveal a novel mechanism by which Lnc Unc-89-AS1 influences BmNPV infection by regulating apoptosis, providing new insights into host antiviral defenses relevant to the prevention and control of silkworm diseases.