Planctomycetota are widely distributed bacteria that play important roles in global element cycles, yet the diversity and ecological functions of their viruses remain poorly understood. Here, we recovered 326 Planctomycetota metagenome-assembled genomes (MAGs) and 96 associated viruses from coastal sediments of the Bohai Sea. These MAGs expand Planctomycetota diversity to 17 classes, including one novel class (currently assigned as class JAKEIC01 in GTDB Release 232) and 13 previously proposed classes. Most associated viruses belonged to Caudovirales, while 41 could not be assigned to known viral groups. Viral genomes encoded auxiliary metabolic genes involved in carbon and sulfur cycling. Analysis of host-virus interactions revealed diverse bacterial defense systems, including restriction-modification, abortive infection, and CRISPR-Cas. We identified three previously uncharacterized protein families associated with known phage resistance strategies, and their expression conferred antiviral resistance or enhanced neighboring defenses. Viral counter-defense strategies were also detected, indicating active host-virus interactions. Together, these findings provide new insights into Planctomycetota-virus interactions and bacterial immunity in marine sediments.
Although associations between the gut microbiota and bone mineral density (BMD) are increasingly recognized, existing evidence largely relies on taxonomic rather than ecological perspectives. How microbial communities function as integrated systems to influence BMD, and the role of serum metabolites, remain unclear. This study integrates gut metagenomic, serum metabolomic, and BMD data from 577 participants in the Taizhou Imaging Study. Employing a guild-based framework, we clustered gut microbiota into putative ecological units (guilds), identified BMD-associated guilds and serum metabolites, and explored mediating effects. Gut microbial diversity did not differ significantly among BMD groups, whereas co-occurrence networks showed different topological patterns: the osteoporotic network exhibited higher connectivity yet lower modularity, suggesting a less organized state. Guild-based analysis identified three candidate BMD-related guilds, and 15 serum metabolites, including amino acids and lipoprotein subfractions, were associated with BMD. Mediation analysis observed a statistical suppression effect in females, where very-low-density lipoprotein-1 triglycerides attenuated the observed positive correlation between a key guild (Guild_17) and its constituent species UBA11524_sp000437595 and BMD (Prop. mediated: − 25.48% and −30.39% at guild and species level). Our findings suggest that BMD is associated with altered gut microbial networks and lipoprotein profiles, providing observational evidence that may inform understanding of osteoporosis.
Chromosome 19 open reading frame 18 (C19orf18) is a protein-coding gene. On the basis of our preliminary findings, C19orf18 is selectively upregulated in the intestine of mice during Salmonella Typhimurium (S. Tm) infection; however, its biological significance and functional role in the course of infection remain unclear. Here, we identify C19orf18 as a host factor associated with S. Tm-induced intestinal inflammation. Consistent results from both in vivo and in vitro experiments demonstrated that loss of C19orf18 function markedly attenuated S. Tm-induced intestinal inflammation and promoted mucosal injury repair. Mechanistically, C19orf18 deficiency was associated with the infection-associated gut ecosystem characterized by enrichment and expansion of Verrucomicrobiota, particularly the beneficial genus Akkermansia, and was associated with amino acid metabolic remodeling characterized by altered tryptophan-associated metabolic profiles. These tryptophan-associated metabolites were associated with epithelial restitution and suppression of inflammatory responses. Collectively, our findings reveal a previously unrecognized mechanism by which C19orf18 modulates host responses to a foodborne enteric pathogen and support a functional relationship among C19orf18-associated microbiota alterations, metabolic changes, and intestinal inflammatory outcomes.
Circadian disruption is a known driver of multisystem pathophysiology, yet how it interfaces with the gut microbiome and systemic metabolism across the life course, and how these interactions are shaped by biological sex, remains poorly defined. We performed longitudinal multi-omics characterization of Bmal1-deficient mice in both sexes across three developmental stages. Ablation of Bmal1 induced core circadian disruption phenotypes, including reduced lifespan, decreased body weight, impaired glucose tolerance, and loss of locomotor rhythmicity, and drove sex- and age-dependent metabolic reprogramming, characterized by divergent insulin sensitivity and systemic lipid profiles. Loss of Bmal1 resulted in pronounced, sex- and age-dependent reorganization of gut microbial community structure and rhythmicity, with specific genera (e.g., norank_f_Muribaculaceae, norank_f_norank_o_Clostridia_UCG-014, Bifidobacterium, Allobaculum) exhibiting altered diurnal oscillations and divergent ecological trajectories across aging. Concurrent plasma metabolomic profiling unveiled sex‑specific metabolic variations and time‑of‑day‑dependent differences in circulating metabolites, suggesting coordinated disruption of microbiome-metabolome dynamics. Targeted quantification further revealed sex‑ and age‑specific alterations in plasma short‑chain fatty acids (SCFAs). Tissue‑specific gene expression analysis in the jejunum, colon, and liver revealed sexually dimorphic and age‑dependent transcriptional reprogramming of clock, barrier, inflammatory, and lipid‑metabolism genes, further underscoring the multi‑organ impact of Bmal1 deficiency. Integrated multi-omics correlation analysis demonstrated that associations between gut microbiome, plasma metabolites, and host glycolipid phenotypes are jointly shaped by sex and developmental age. Our findings identify aging and biological sex as pivotal, non-redundant ecological modifiers of circadian-associated host-microbiome interactions, underscoring the necessity of incorporating these variables into mechanistic models and translational strategies for circadian-related disorders.
Microbial constituents in the gastrointestinal tract, the urine and prostate tissue are being linked with clinical differences in prostate cancer, and a recent meta-analysis has linked periodontal disease to this cancer. Several hypotheses exist regarding how specific bacteria can contribute towards the development of prostate cancer. Recovering microbial genomes, and their genomic features, from clinical samples and investigating fine-scale taxonomy is a critical first step in investigating causality. Here, we describe the microbial diversity of samples associated with prostate cancer. Metagenomic assembly of non-human reads from the PanProstate Cancer Group, derived from blood, saliva samples and prostate tissue whole-genome data (N = 247), successfully reconstructed 249 highly complete bacterial genomes, predominantly from oral samples. Our data, reveals eighteen bacterial species from the oral cavity without species level classification, while demonstrating a wide range of known species. This approach enables us to gain additional insights of the microbes in cancer patients at no additional sequencing cost and has the potential to reveal new links that could improve our understanding of cancer initiation and development.
