Microbiological research最新文献

Fruiting bodies of mushroom-forming fungi (Agaricomycetes) exhibit the highest degree of multicellular complexity in fungi, yet the molecular underpinnings of their developmental programs remain incompletely understood. Here, we characterize gcd1, a gene encoding a transcription factor in the Con7 subfamily of C2H2-type zinc finger proteins. This subfamily has previously been implicated in pathogenic morphogenesis in Ascomycota, but its role in Agaricomycetes has not previously been addressed. In Coprinopsis cinerea, CRISPR/Cas9-mediated deletion of gcd1 resulted in strains with severely impaired fruiting body morphogenesis, with malformed cap, stipe, and gill tissues. Gcd1 deletion strains lacked universal veil, resembling species with open (gymnocarpous) development. We find that GCD1/Con7 homologs are widely distributed in most Dikarya species and are mostly encoded by a single gene in each species' genome. Transcriptome analyses identified several misregulated genes in the Δgcd1 mutant, which pinpoint potential mechanisms underlying its developmental defects as well as provided insights into the morphogenesis of mushroom fruiting bodies. These findings establish GCD1 as a key regulator of multicellular development in C. cinerea and broaden the known functions of Con7-like transcription factors to include fruiting body morphogenesis in Agaricomycetes. Overall, our results and the morphogenetic role of Con7-like transcription factors of Ascomycota suggest functional conservation over half a billion years of evolution.

Xenophagy, a form of selective autophagy targeting intracellular pathogens, constitutes a central arm of cell-autonomous innate immunity. This review synthesizes recent advances in the molecular regulation of xenophagy, emphasizing ubiquitin-dependent and ubiquitin-independent cargo tagging, receptor redundancy and context dependence, and post-translational control of autophagy-related 8/microtubule-associated protein 1 light chain 3 (ATG8/MAP1LC3/LC3) engagement. We discuss how pathogens exploit or evade xenophagic defenses at multiple checkpoints, cargo recognition, receptor recruitment, autophagosome biogenesis, and lysosomal fusion, highlighting mechanistically defined bacterial and viral countermeasures. Attention is given to the distinction between canonical xenophagy and non-canonical LC3-associated phagocytosis (LAP), clarifying their divergent regulatory logic and functional outcomes. We further examine the integration of xenophagy with innate immune signaling, antigen processing and presentation, and intercellular communication via exosomes, thereby linking intracellular pathogen restriction to adaptive immunity. Emerging discovery platforms, including multi-omics and clustered regularly interspaced short palindromic repeats (CRISPR-based) genetic screens, are evaluated for their potential to uncover novel xenophagy regulators. Finally, we critically assess translational opportunities for xenophagy-targeted host-directed therapies, emphasizing pathogen-specific context, tissue-restricted delivery, and the risks of non-selective autophagy modulation. Together, this review provides a mechanistic and translational framework for understanding xenophagy as a dynamic, context-dependent immune defense pathway rather than a uniformly protective degradative process.

In this study, the effects of Pseudomonas putida strain XMS-1 and its sodium alginate (SA)-producing gene algD deletion mutant (∆algD) on cadmium (Cd) immobilization in solution, and Cd availability and uptake in lettuce plants and mechanisms involved in the contaminated soils were investigated. Compared with XMS-1, ∆algD increased the solution Cd concentration by 57 % and reduced the cell surface-adsorbed and intracellular Cd contents by 44-57 % after 36 h of incubation. Compared with XMS-1, ∆algD significantly decreased the lettuce biomass, iron/manganese oxide- and organic matter-bound Cd contents, pH values, and polysaccharide and mineral-associated organic carbon contents and increased the exchange of Cd and lettuce leaf Cd contents in the soils. Furthermore, compared with XMS-1, ∆algD significantly reduced the relative abundances of Cd-immobilizing related abundant (Knoellia, Pseudomonas, Lysobacter, Microbacterium, and Flavisolibacter) and rare (Saccharothrix, Pajaroellobacter, Dyadobacter, Stenotrophomonas, Candidatus Koribacter, and Mumia) genera and functional genes mnxG, cumA, mnp, and epsA involved in manganese oxidation, ferromanganese nodule formation, and exopolysaccharide production in the rhizosphere soils of lettuce plants compared to XMS-1. Correlation analysis revealed negative relationships between the relative abundances of these bacterial populations and Cd uptake in lettuce tissues. These findings suggest the significant effects of algD in XMS-1 on reducing Cd availability and accumulation in lettuce through enriching the Cd-immobilizing related bacterial communities and functional genes in the contaminated soils. Our findings offer new insights into the mechanisms underlying algD-mediated reduction in Cd accumulation in lettuce by XMS-1, laying a crucial foundation for the use of SA-producing bacteria to ensure safe vegetable production in the Cd-contaminated soils.

Obesity-driven systemic inflammation is a critical contributor in the progression of metabolic diseases. While lactic acid bacteria (LAB) are recognized for countering diet-induced obesity, their specific role in mitigating the associated inflammatory pathways requires further elucidation. This study investigated the capacity of a novel LAB strain, Lactiplantibacillus plantarum BGI-N6 (N6), to alleviate obesity and its related inflammatory responses in a high-fat diet (HFD)-fed Sprague-Dawley (SD) rat model. N6 supplementation effectively attenuated body weight gain, fat deposition, and liver steatosis, while concurrently improving systemic metrics such as blood lipid profiles. Crucially, the treatment significantly reduced HFD-induced systemic inflammation and oxidative stress. Analysis of the gut microbiota demonstrated that N6 administration modulated gut microbiota composition, enhancing β-diversity and reducing the abundance of pro-inflammatory taxa, including Sutterella wadsworthensis, Bilophila wadsworthia, and Holdemania filiformis. These structural changes were accompanied by metabolic shifts, specifically an increased production of butyric and valeric acids and a decrease in propionic acid. Furthermore, N6 specifically downregulated bacterial biosynthesis pathways for lipopolysaccharide (LPS), an effect attributed to the reduced abundance of key gram-negative species such as Sutterella wadsworthensis, resulting in significantly lower serum LPS levels. Correlation analyses confirmed the strong association of these microbial and metabolic changes with improved metabolic and inflammatory parameters. Collectively, these findings demonstrate that N6 ameliorates obesity-induced inflammation and oxidative stress through a multi-faceted mechanism involving gut microbiota restructuring, SCFA modulation, and LPS reduction, underscoring its potential as a therapeutic probiotic for metabolic disorders.

Phage therapy is being used to combat pathogenic bacterial infections that threaten plant, animal, and human health. However, its application remains limited by high host specificity and the emergence of bacterial resistance. In this study, we addressed the key issues in phage therapy using rice bacterial blight pathogen Xanthomonas oryzae pv. oryzae (Xoo) strain N1 and its lytic phage NP1. Strain N1 acquired resistance to the phage NP1 through mutations and downregulation of lipopolysaccharide (LPS) biosynthesis genes. A directed evolution assay using phage NP1 and the resistant strain N1R resulted in the development of phage E12-2, which overcame bacterial resistance, expanded its host range and improved bacterial suppression by targeting alternative LPS binding sites. Moreover, genome analysis identified two amino acid substitutions (V303L and G317V) in its tail fiber protein. Additionally, phage E12-2 improved disease control efficiency by 51 % compared to the wild-type phage NP1 and induced plant immunity in a plant disease model. These findings enhance our understanding of how bacteria-phage evolution shapes the dynamics of phage therapy in plants.