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Zhao, J.-X.

Publications and source records attributed to Zhao, J.-X..

3 recordsLinked to original sources

Toxoplasma gondii disrupts vitamin B and K2 biosynthetic pathways in feline gut microbiota: microbial adaptation

Vitamins B and K2 (menaquinone) are critical for microbial and host processes, but their biosynthesis in feline gut microbiota and modulation by Toxoplasma gondii remain unclear. We assembled 1,553 high-quality feline intestinal bacterial genomes from metagenomic and public data to study vitamin B and K2 biosynthesis. We identified 86,829 genes and 159 enzymes, revealing regional differences in gene and species diversity for vitamin production. Among these, 782 genomes supported de novo synthesis of at least one vitamin. T. gondii infection altered synthesis pathways: early infection boosted pyridoxine and riboflavin synthesis in the small intestine, while menadione synthesis declined in both intestines. Actinomycetota and Campylobacterota were key to menaquinone biosynthesis, with T. gondii disrupting canonical pathways and activating alternatives. These findings shed light on the complex interplay between host, parasite, and microbiota in shaping vitamin biosynthesis, offering new perspectives for maintaining feline gut health during parasitic infection.

microbiology↗

Expanding the chicken gut virome: Uncovering viral diversity, host interactions, and regional variations across the intestinal tract

Chicken gastrointestinal virome comprises a complex and diverse viral community with significant implications for host health and microbiome function. We analyzed 3,312 publicly available chicken gut metagenomic datasets to establish the chicken gastrointestinal virome collection (CGVD), which includes 39,380 non-redundant viral operational taxonomic units (vOTUs); notably, 84.90% (33,433/39,380) represent novel sequences absent from current databases. Over half of the CGVD vOTUs were classified as bacteriophages, predominantly from the order Caudovirales. The predicted hosts were mainly prokaryotes, particularly Bacillota and Bacteroidota, revealing a multifaceted landscape of virus-host interactions. Many vOTUs infected multiple bacterial phyla, indicating high adaptability and broad ecological impact. In addition, lifestyle prediction showed that 28.28% (11,137 /39,380) of the vOTUs in CGVD were identified as lytic phages. Functional annotation demonstrated that viral genes contribute to key metabolic processes, including nucleotide and amino acid metabolism, thereby facilitating viral replication and host adaptation. The detection of auxiliary metabolic genes and carbohydrate-active enzymes underscores the role of viruses in modulating the gut microbiome. Although antibiotic resistance genes and mobile genetic elements were present, their contribution to horizontal gene transfer appears limited. Additionally, marked regional differences in virome composition were observed between the small and large intestines, particularly in the abundance of families such as Siphoviridae and Myoviridae. CGVD not only highlights the key role of viruses in shaping the chicken gut microbiome and influencing microbial dynamics and metabolic pathways, but also provides new resources and insights for future research.

microbiology↗

Lactylation-driven FTO-mediated m6A modification of CDK2 aggravates diabetic microvascular anomalies

Diabetic retinopathy (DR) is a leading cause of irreversible vision loss in working-age populations. FTO is an N6-methyladenosine (m6A) demethylase that participates in various biological events, while its role in DR remains elusive. Herein, we detected elevated FTO expression in retinal proliferative membranes of DR patients. FTO promoted endothelial cell (EC) cell cycle progression and tip cell formation to facilitate angiogenesis in vitro, in mice and in zebrafish. FTO also regulated EC-pericyte crosstalk to trigger diabetic microvascular leakage, and mediated EC-microglia interactions to induce retinal inflammation and neurodegeneration in vivo and in vitro. Mechanistically, FTO affected EC features via modulating CDK2 mRNA stability in an m6A-YTHDF2-dependent manner. FTO up-regulation under diabetic conditions was driven by lactate mediated histone lactylation. FB23-2, an inhibitor to FTOs m6A demethylase activity, suppressed angiogenic phenotypes in vivo and in vitro. Noteworthy, we developed a nanoplatform encapsulating FB23-2 for systemic administration, and confirmed its targeting and therapeutic efficiencies in mice. Collectively, our study demonstrated that FTO coordinates EC biology and retinal homeostasis in DR, providing a promising nanotherapeutic approach for DR.

cell biology↗