Jul 2026· Journal of Invertebrate Pathology· Vol 219, pp.
108708
· 0 citations· 45 references
Medicine
TL;DR
It is demonstrated that lnc5714 suppresses the expression of BmMRPL4 by downregulating its mRNA level, thereby weakening mitochondrial energy output in host cells and restricting the replication of N. bombycis.
Abstract
Pebrine caused by Nosema bombycis is a devastating infectious disease that severely constrains the development of the sericulture industry. Because this pathogen is highly dependent on host-derived energy and nutrients, identifying key factors that regulate host metabolism is crucial for elucidating the mechanisms of disease resistance. In this study, we identified and cloned a long non-coding RNA, lnc5714, that was differentially induced in response to N. bombycis infection. Subcellular localization analysis showed that lnc5714 was predominantly distributed in the cytoplasm. Functional assays demonstrated that overexpression of lnc5714 significantly inhibited the replication of N. bombycis, whereas knockdown of lnc5714 promoted its proliferation, confirming that lnc5714 is a resistance-associated factor. Network prediction and experimental validation further revealed that the potential target gene of lnc5714 is the mitochondrial ribosomal protein BmMRPL4. Further analyses confirmed that the expression of BmMRPL4 was negatively regulated by lnc5714, and that the expression level of BmMRPL4 directly affected intracellular ATP levels: overexpression of BmMRPL4 increased ATP content and promoted pathogen proliferation, whereas its knockdown produced the opposite effect. Taken together, our findings demonstrate that lnc5714 suppresses the expression of BmMRPL4 by downregulating its mRNA level, thereby weakening mitochondrial energy output in host cells and restricting the replication of N. bombycis. This study provides a new theoretical basis for the identification of disease-resistance molecular markers and the genetic improvement of silkworms.
Antimicrobial peptides (AMPs) are critical components of the innate immune system in insects, but their regulation and contribution to antiviral defence remain poorly understood. In this study, we investigated the expression, antiviral activity and regulation of Bombyx mori Lebocin-3 (BmLEB3) during infection with Bombyx mori cytoplasmic polyhedrosis virus (BmCPV). BmLEB3 expression was markedly induced following BmCPV infection in the silkworms. RNAi-mediated knockdown of BmLEB3 increased the transcriptional level of viral marker gene vp1 in BmN cells, whereas overexpression led to the inhibition of viral replication in BmN cells. Mechanistically, BmCPV induced the expression of the pattern-recognition receptor BmPGRP-S1 and the transcription factor BmRelish, and silencing of either gene reduced BmLEB3 expression, suggesting that immune deficiency (IMD)-associated signalling contributes to BmLEB3 regulation. Moreover, BmLEB3 was induced by 20-hydroxyecdysone (20E) treatment, further strengthening its antiviral effect. Molecular docking analysis revealed a potential interaction between 20E and BmPGRP-S1, indicating a possible hormonal modulation of IMD-associated AMP expression. Collectively, our results identify BmLEB3 as a virus-responsive AMP and suggest that its expression is modulated by IMD-associated signalling and hormonal cues during BmCPV infection in B. mori. These findings provide insight into the molecular regulation of antiviral immune responses in the silkworm and provide a basis for improving disease resistance in sericulture against microbial pathogens.
M. Awais, Nasir Mehmood, Wensheng Yu et al.· Insect molecular biology (Pr...· 0 citations
The SUN family protein MoSun4 in Magnaporthe oryzae has been previously implicated in mitophagy and has potential as a target for reducing rice blast, but its role as a secreted protein remains poorly understood. In this study, signal peptide prediction and yeast secretion assays confirmed MoSun4 signal peptide function, and co-localization revealed the localization of the extra-invasive hyphal membrane (EIHM)-associated apoplastic compartment or matrix, establishing MoSun4 as a secreted protein. In addition, deletion of the MoSUN4 gene reduced the hyphal growth, conidiation and virulence of M. oryzae. We further showed that MoSun4 is involved in regulating the expression of virulence-related genes, including multiple genes involved in cell wall degradation (eglC, eglD), secondary metabolism (gliK), and melanin biosynthesis (SDH1, BUF1, Cmr1, ALB1). Collectively, our study reveals that MoSun4 is a secreted protein that contributes to pathogenicity and is associated with altered expression of virulence-related genes, providing new insights into the functions of SUN family proteins.
Huimin Li, Zhenhe Su, Xiaomeng Liu et al.· Journal of Fungi· 0 citations
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.
Xin Jia, Min Cai, Yu Xiao et al.· Journal of Invertebrate Path...· 0 citations
Nervous necrosis virus (NNV) is a major viral pathogen that causes viral nervous necrosis in a wide range of fish species and poses a serious threat to global aquaculture. However, the antiviral responses of mandarin fish (Siniperca chuatsi) to NNV infection remain poorly understood. In this study, we investigated host antiviral responses using Chinese perch brain (CPB) cell line and in vivo infection models. Transcriptome sequencing of red-spotted grouper nervous necrosis virus (RGNNV)-infected CPB cells revealed extensive transcriptional reprogramming, with numerous interferon-stimulated genes (ISGs) significantly upregulated. Comparative transcriptomic analysis across multiple teleost species identified a conserved set of ISGs induced during RGNNV infection, including CMPK2, RSAD2, DHX58, IRF3, and EPSTI1. Among these genes, CMPK2 showed strong induction in both infected CPB cells and mandarin fish brain tissues. Functional assays further demonstrated that CMPK2 overexpression significantly inhibited RGNNV replication in CPB cells and was accompanied by increased expression of several interferon-related genes. These findings provide the first functional evidence that CMPK2 restricts RGNNV infection in S. chuatsi. Our study highlights a conserved interferon-responsive antiviral module in teleost fish and identifies CMPK2 as a potential antiviral effector involved in host defense against RGNNV infection.
Chanxia Qin, Jinlong Huang, Linmiao Li et al.· Developmental and Comparativ...· 0 citations
Ribosomal protein L11 (RPL11) plays important roles in ribosome biogenesis and stress responses, yet its antiviral function remains poorly understood. This study characterized BmRPL11 and its role in Bombyx mori nucleopolyhedrovirus (BmNPV) infection. BmRPL11 is evolutionarily conserved and shares high sequence homology and protein structure with RPL11 from other species. Tissue expression profiling showed predominant BmRPL11 expression in silk glands and the fat body, with upregulation after BmNPV infection. Functional assays demonstrated that BmRPL11 knockdown enhanced, whereas overexpression suppressed, BmNPV proliferation in BmN cells and silkworm larvae. Mechanistically, BmNPV infection induced nuclear export of BmRPL11 and was associated with enhanced apoptosis, while autophagy-related genes were not markedly affected by BmRPL11 knockdown. IP-MS identified candidate BmRPL11-interacting proteins during infection, including RPL5, whereas a canonical murine double minute 2 (MDM2) homologue was not detected. These findings identify BmRPL11 as an antiviral factor in silkworms, potentially acting through an apoptotic rather than an autophagic pathway.
Junming Xia, Wensheng Yu, Zexiang Huang et al.· Journal of Agricultural and...· 0 citations
The sustainable development of shrimp aquaculture is significantly compromised by Vibrio parahaemolyticus infections. Identifying host resistance genes and characterizing their immunological roles are essential for developing effective disease control strategies. In this study, we conducted a comparative transcriptomic analysis of intestinal tissues from Penaeus vannamei exhibiting varying degrees of pathological damage post-V. parahaemolyticus challenge to identify key resistance genes. KEGG enrichment analysis revealed that the ABC transporter pathway was markedly enriched among upregulated genes in both the 9 h vs 0 h and 48 h vs 0 h comparison groups. Based on the expression profiles and domain characteristics of genes within this pathway, the full transporter PvABCA3, half transporter PvABCC1, and soluble protein PvABCF2 were selected for RNAi assays. The result indicated that silencing PvABCF2, but not PvABCA3 and PvABCC1, significantly increased mortality, tissue damage, and Vibrio load in V. parahaemolyticus-challenged shrimp. Further investigation revealed that PvABCF2 silencing substantially suppressed the expression of antimicrobial peptides (AMPs), components of the proPO-activating system, and key genes involved in the JAK-STAT and NF-κB signaling pathways. These findings suggested that the increased susceptibility of shrimp to V. parahaemolyticus following PvABCF2 silencing may be associated with downregulation of these specific immune-related genes. Moreover, one SNP within PvABCF2 was found to be markedly associated with resistance to V. parahaemolyticus via SNP association analysis. Collectively, these results suggested that PvABCF2 was involved in defense response against V. parahaemolyticus and identified a potential molecular marker for disease-resistant breeding.
Shuang-Shuang Luo, Lin-Lin Shi, Qing-yun Liu et al.· Genomics· 0 citations
