Outbreaks and epidemics of RNA viruses represent a serious threat to human health. The retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) signaling pathway plays a pivotal role in host resistance to viral infections. RLRs recognize the RNA produced after viral invasion, initiating the activation of the RLR signaling pathway to combat viral infection. Abnormal activation of this pathway is linked to the development of chronic inflammation, damage to immune organs, and autoimmune diseases. To prevent the disruption of RLR signaling pathway activation, the body has established a comprehensive regulatory system with the objective of stabilizing the RLR signaling pathway. Protein methylation represents a significant post-translational modification of proteins, playing a pivotal role in numerous biological processes. The methylation of molecules in the RLR signaling pathway has been demonstrated to be indispensable for the body to regulate the RLR signaling pathway. This paper presents a comprehensive review of the latest research findings on the role of protein methylation in regulation of the RLR signaling pathway, offering novel insights into the host regulation of the RLR signaling pathway in combatting viral infection.

DNA methylation is an important way of epigenetic regulation in bacteria. Alphaproteobacteria methylate DNA by using the cell cycle-regulated DNA methyltransferase (CcrM). CcrM does not contain a functional unit of restriction endonuclease, thus belonging to an orphan methyltransferase. By methylating adenine in DNA sequences, CcrM influences the interaction between DNA and proteins, regulates the expression of numerous genes, and is crucial for the regulation of processes such as the cell cycle of Alphaproteobacteria. We reviewed the function, structure, and epigenetic regulation of CcrM, clarified the mechanisms of CcrM in DNA recognition, catalysis, and activity regulation, summarized the mechanism by which the global cell-cycle regulator (GcrA) utilizes the methylation signals produced by CcrM to regulate gene expression, and provided an outlook on the potential future research directions of CcrM, providing a reference for further in-depth study of the epigenetic regulation mechanisms in bacteria.

Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease around the world, and it has a complex disease progression. Recent studies have demonstrated that gut microbiota (GM) plays a crucial role in the pathogenesis of NAFLD. The theory of gut-liver axis provides a theoretical basis for understanding the relationship between GM and the liver. Dysbiosis of GM leads to immune dysfunction, inflammatory responses, damaged gut barrier, and insulin resistance, all of which promote the development and progression of NAFLD. Furthermore, GM can participate in the development and progression of NAFLD through endotoxemia and abnormal metabolism of short chain fatty acids, bile acids, and choline. How to mitigate NAFLD by modifying GM has become the focus of current research, and the measures include fecal microbiota transplantation, probiotics, prebiotics, Chinese herbal medicines, and lifestyle interventions. The review focuses on the impact of the pathological state of GM on NAFLD and discusses the research progress in GM-targeted therapy for NAFLD. It is expected to provide new strategies and targets for the prevention and treatment of NAFLD.

Streptomyces are deeply studied and applied in the biocontrol of plant diseases. Streptomyces are widely distributed in soil, ocean and plant tissue. Streptomyces and the bioactive metabolites produced by Streptomyces exhibited antifungal, antibacterial, antivirus, nematicidal, pesticidal and herbicidal effects. The biocontrol mechanisms of Streptomyces against plant diseases, including antifungal activity, mycoparasitism, inducing resistance, enhancing plant growth, producing volatile organic compounds were summarized. The commercialized biocontrol agents developed based on Streptomyces were introduced. The research on Streptomyces-based biocontrol agents is limited in China, and the development and promotion of such agents could decrease the use of chemical fungicides and promote the environmental-friendly sustainable development of agriculture.

Akkermansia muciniphila, a major gut microorganism, has garnered significant attention for its involvement in the regulation of glucose and lipid metabolism. Glucose and lipid metabolic disorders, characterized by hyperglycemia and dyslipidemia, are caused by multiple factors. These disorders are not only prevalent globally but also increasingly common among young people in China, representing a major public health concern. This review systematically elaboratesthe research progress in A. muciniphila and glucose and lipid metabolism from the perspective of its mechanisms of action. Specifically, the review summarizes the regulatory pathways through which A. muciniphila influence glucose and lipid metabolism, assesses how pharmaceuticals that enhance A. muciniphila abundance affect metabolic parameters, and discusses advances in the bioengineering of A. muciniphila. By synthesizing current research findings, this review aims to provide valuable insights for understanding glucose and lipid metabolic disorders and developing novel therapeutic approaches for related diseases.

[Objective] This study investigates the effects of various diets on the structure and diversity of the fungal community in the tobacco beetle Lasioderma serricorne, aiming to provide a theoretical basis for developing green control strategies for stored-product pests through microbial regulation. [Methods] The PacBio SMRT platform was used for full-length internal transcribed spacer (ITS) amplicon sequencing, on the basis of which the community structure characteristics of fungi in L. serricorne were compared among three groups: artificial feed (SL), tobacco domestication (YC), and wild environment (WF). Additionally, culturable fungi were isolated via the culture method, and the tissue expression pattern of the core symbiotic fungus Symbiotaphrina kochii was localized by RT-qPCR. [Results] SL, YC, and WF groups contained 35, 32, and 15 operational taxonomic units (OTUs), respectively. The core OTUs shared by the three groups accounted for 31.43%, 34.38%, and 73.33% in SL, YC, and WF groups, respectively. The Sobs index of the SL group was 29.00±1.13, which was higher than those of the YC group (16.17±2.30) and WF group (12.33±1.33) (P<0.001). Symbiotaphrina was the core functional group shared by the three groups, and its relative abundance was more than 81.000 0% in all the three groups. Aspergillus and Xeromyces were the characteristic genera of the SL and YC groups, while Symbiotaphrinabuchneri and Symbiotaphrina microtheca formed the evolutionary clades specific to the YC and WF groups. Eight Ascomycota strains were isolated via the culture method, belonging to three genus: Symbiotaphrina (three strains), Talaromyces (three strains), and Penicillium (two strains). Tissue-specific expression analysis confirmed the higher expression level of S. kochii in mycetocytes (10.42±1.03) than in the fat body (0.74±0.08) and midgut (0.31±0.01) (P<0.001), validating its intracellular colonization. [Conclusion] This study for the first time reveals that diets regulate the fungal community assembly in L. serricorne through a “nutrient-microbiota” interaction network and demonstrates the pivotal role of Symbiotaphrina in adaptive evolution of the host. These findings establish a theoretical foundation and provide critical targets for developing precision pest control technologies based on targeted modulation of microbial interaction networks.

The gut microbiota plays a pivotal role in regulating animal health, and its structure and function can be significantly modulated by fermented feed. However, the lack of cross-species comparative studies has hindered a comprehensive understanding of the universal mechanisms underlying fermented feed-mediated microbial regulation. [Objective] To integrate multi-species data for deciphering cross-species regulatory patterns of fermented feed on gut microbiota and elucidating universal functional optimization and host-specific mechanisms. [Methods] We aggregated 464 gut microbiome datasets from pigs, cattle, chickens, and geese. The alpha/beta diversity analyses, linear discriminant analysis effect size (LEfSe), BugBase, and network analyses were employed to assess the diversity, differentially enriched genera, pathogenicity, and interactions of the gut microbiota. [Results] Fermented feed markedly reduced the alpha diversity of gut microbiota in monogastric animals (pigs, chickens, and geese) but not in ruminants (cattle). Although the beta diversity of gut microbiota remained statistically stable in different animals, fermented feed enriched probiotics (e.g., Lactobacillus and Faecalibacterium) while suppressing pathogens (e.g., Campylobacter and Brachyspira) to significantly diminish the pathogenic potential. Network analysis revealed enhanced connectivity, increased network density, reduced modularity, and improved community synergy in fermented feed groups. Host-specific responses were identified: Lactobacillus dominated in pigs, Akkermansia in cattle, and Flavonifractor in chickens. [Conclusion] Fermented feed modulates gut microbiota through a pattern coupling consistent response optimization with host-specific responses, selectively enriching keystone taxa to improve the specific function and reduce the pathogenicity. This study provides theoretical foundations for developing host-tailored fermented feed strategies.

Foot-and-mouth disease (FMD) is a highly contagious disease caused by foot-and-mouth disease virus (FMDV) in cloven-hoofed animals. FMDV is a single-stranded positive-sense non-enveloped RNA virus with icosahedral symmetry. FMDV can cause innate and adaptive immunity of the host, and it has evolved a variety of immune escape ways. The FMDV infection is a complicated process involving various host proteins. However, the related mechanisms remain largely unknown. Voltage dependent anion-selective channel 2 (VDAC2) is a mitochondrial channel protein, and the specific mechanism by which VDAC2 regulates FMDV replication remains unclear. [Objective] To confirm the regulatory effects between VDAC2 and FMDV and reveal the molecular mechanism by which VDAC2 inhibits FMDV replication. [Methods] The subcellular localization of VDAC2 was determined by the indirect immunofluorescence assay. The effects of FMDV on the translation and transcription levels of VDAC2 were determined by Western blotting and qPCR, respectively. The effect of VDAC2 overexpression on FMDV replication in BHK-21 cells was measured based on the virus titer. The effects of VDAC2 overexpression and knockdown on the levels of IL-1β, ISG15, OAS1, mtDNA, and gDNA during FMDV infection were evaluated by qPCR. [Results] VDAC2 was localized in the cytoplasm. FMDV infection down-regulated the expression of VDAC2. The overexpression of VDAC2 inhibited FMDV replication in a dose-dependent manner, while the knockdown of VDAC2 promoted FMDV replication. The overexpression of VDAC2 enhanced FMDV-induced interferon-I (IFN-I) response, while the knockdown of VDAC2 inhibited FMDV-induced IFN-I response. In addition, the overexpression of VDAC2 increased the release of mtDNA. [Conclusion] FMDV infection can downregulate the transcription and translation of VDAC2, as VDAC2 can exert antiviral effects by regulating mtDNA release and promoting the expression of antiviral factors such as IL-1β, ISG15, and OAS1. This study indicates that upon FMDV infection, host cells can regulate the virus replication by enhancing IFN-I response via VDAC2 to exert antiviral effects.

[Objective] To investigate the role of lmo2300 in oxidative stress resistance and infection of Listeria monocytogenes. [Methods] With L. monocytogenes 1/2 a serotype EGD-e as the parent strain, the lmo2300-deleted strain and complementary strain were constructed by homologous recombination. The growth, motility, oxidative stress resistance, minimum inhibitory concentration and reductase activity of Δlmo2300 were evaluated. The adhesion, invasion, proliferation, and intercellular migration abilities of the Δlmo2300 strain was assessed using cell models. The transcriptional levels of thioredoxin-related genes and major virulence genes in Δlmo2300 were detected with RT-qPCR. [Results] PCR identification and DNA sequencing confirmed the successful construction of Δlmo2300 and CΔlmo2300. Deletion of lmo2300 did not affect the bacterial growth, motility, antibiotic susceptibility, adhesion, invasion or intracellular proliferation. However, the Lmo2300 protein possesses reductase activity, and the transcriptional levels of the thioredoxin gene lmo1903 and grx are significantly upregulated in the Δlmo2300 mutant. And markedly improved resistance to oxidative substances, including H₂O₂, diamide, CdCl₂, and MnSO₄ compared with the wild type. The Δlmo2300 mutation significantly enhanced intercellular migration ability, accompanied by an approximately 8-fold upregulation of the actA gene transcription, which is consistent with the enhanced intercellular migration ability. [Conclusion] This study demonstrates that lmo2300 plays a critical role in modulating the oxidative stress resistance and intercellular migration of L. monocytogenes, providing novel insights into the infection biology and adaptive responses of L. monocytogenes to host-derived oxidative challenges.

Cotton Verticillium wilt, caused by the soil-borne fungal pathogen Verticillium dahliae, is a devastating disease that severely impacts global cotton production. [Objective] To investigate the biocontrol potential and mechanism of endophytic Pseudomonas sp. NWSUAF303 against cotton Verticillium wilt and provide novel microbial resources for managing soil-borne diseases in cotton. [Methods] The strain was identified by phylogenetic analysis based on 16S rRNA gene sequences and phenotypic characterization. Its antifungal spectrum was evaluated via dual-culture and volatile organic compounds (VOCs) inhibition assays. VOCs were detected by headspace solid-phase microextraction coupled with gas chromatography-mass spectrometry (HS-SPME-GC-MS). Pot experiments were carried out to assess the disease control efficacy of the strain. RT-qPCR and enzymatic activity assays were employed to elucidate the resistance mechanism of the strain against cotton Verticillium wilt. [Results] Strain NWSUAF303 was identified as Pseudomonas alvandae, exhibiting plant growth-promoting properties including nitrogen fixation, phosphate solubilization, and indole-3-acetic acid (IAA) production. Its non-volatile metabolites inhibited six phytopathogenic fungi, whereas VOCs demonstrated broader antifungal spectrum against seven pathogens, showing the inhibition rates >95% against Sclerotinia sclerotiorum and of 89.27% against V. dahliae 592. The VOCs of this strain downregulated the expression of virulence genes (VdPR1, Vdpf, and VdGAL4) in V. dahliae (P<0.05). Three key antifungal VOCs were identified, including 2,3-butanedione, 2-nonanol, and 6-methyl-2-heptanol, with the inhibitory effect of 2,3-butanedione on V. dahliae being first reported. Pot experiments revealed the control efficacy of 54.40% against Verticillium wilt, which was comparable to that of carbendazim. Strain NWSUAF303 activated the salicylic acid/jasmonic acid (SA/JA) signaling pathway, upregulating the expression of defense-related genes GhPAL, Gh4CL, and GhCHI (P<0.01), while enhancing the activities of peroxidase (POD), polyphenol oxidase (PPO), and superoxide dismutase (SOD). [Conclusion] P. alvandae NWSUAF303 combats Verticillium wilt through dual mechanisms: producing novel antifungal VOCs and activating systemic resistance via SA/JA signaling and defense enzyme coordination. With broad-spectrum antifungal activity and plant growth-promoting properties, this strain represents a promising biocontrol agent for sustainable management of cotton Verticillium wilt.