ArticlePloS one2017
Analysis of the complete genome sequence of Nocardia seriolae UTF1, the causative agent of fish nocardiosis: The first reference genome sequence of the fish pathogenic Nocardia species.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 64 citations in OpenAlex.
- Isolation, Identification and Whole-Genome Sequencing of aAnimals : an open access journal from MDPI · 2026Article
- Whole-genome sequencing and analysis of Nocardia veterana isolates from keratitis patients.Molecular genetics and genomics : MGG · 2026Article
- Genome architecture reveals hidden strain-level diversity in the highly conserved fish pathogen Nocardia seriolae.Access microbiology · 2026Article
- Comparative genomics ofFrontiers in microbiology · 2026Article
- Research progress on clinical challenges and prevention strategies of drug-resistantFrontiers in public health · 2026Review
- Surface display of Nocardia seriolae HRP1 on Bacillus subtilis and its application as live vaccine for largemouth bass.Scientific reports · 2025Article
- Genomic characteristics, virulence potential, antimicrobial resistance profiles, and phylogenetic insights into Nocardia cyriacigeorgica.Annals of clinical microbiology and antimicrobials · 2025Article
- Discovery of Novel Diagnostic Biomarkers for Common PathogenicPathogens (Basel, Switzerland) · 2025Article
- Pathogenicity and whole-genome analysis of aFrontiers in microbiology · 2025Article
- Effects of sulfamethoxazole and copper on the natural microbial community from a fertilized soil.Applied microbiology and biotechnology · 2024Article
- Unravelling the genomic secrets of bacterial fish pathogens: a roadmap to aquaculture sustainability.Molecular biology reports · 2024Review
- Biological characteristics and pathogenicity comparison ofFrontiers in veterinary science · 2024Article
- Comparison of Clinical Characteristics and Treatment Outcome Between Localized and Disseminated Nocardiosis in a Tertiary Hospital in China.Infection and drug resistance · 2024Article
- Isolation and Complete Genome Sequencing of NS-I, a Lytic Bacteriophage Infecting Fish Pathogenic Strains ofPHAGE (New Rochelle, N.Y.) · 2023Article
- Design of a multi-epitope vaccine against six Nocardia species based on reverse vaccinology combined with immunoinformatics.Frontiers in immunology · 2023Article
- Updated Review onClinical microbiology reviews · 2022Review
- Review
- Comparative genomics ofMicrobial genomics · 2022Article
- Insights from the comparative genome analysis of natural rubber degradingBioinformation · 2021Article
- Genomic Virulence Features of Two Novel SpeciesMicroorganisms · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nocardiosis caused by Nocardia seriolae is one of the major threats in the aquaculture of Seriola species (yellowtail; S. quinqueradiata, amberjack; S. dumerili and kingfish; S. lalandi) in Japan. Here, we report the complete nucleotide genome sequence of N. seriolae UTF1, isolated from a cultured yellowtail. The genome is a circular chromosome of 8,121,733 bp with a G+C content of 68.1% that encodes 7,697 predicted proteins. In the N. seriolae UTF1 predicted genes, we found orthologs of virulence factors of pathogenic mycobacteria and human clinical Nocardia isolates involved in host cell invasion, modulation of phagocyte function and survival inside the macrophages. The virulence factor candidates provide an essential basis for understanding their pathogenic mechanisms at the molecular level by the fish nocardiosis research community in future studies. We also found many potential antibiotic resistance genes on the N. seriolae UTF1 chromosome. Comparative analysis with the four existing complete genomes, N. farcinica IFM 10152, N. brasiliensis HUJEG-1 and N. cyriacigeorgica GUH-2 and N. nova SH22a, revealed that 2,745 orthologous genes were present in all five Nocardia genomes (core genes) and 1,982 genes were unique to N. seriolae UTF1. In particular, the N. seriolae UTF1 genome contains a greater number of mobile elements and genes of unknown function that comprise the differences in structure and gene content from the other Nocardia genomes. In addition, a lot of the N. seriolae UTF1-specific genes were assigned to the ABC transport system. Because of limited resources in ocean environments, these N. seriolae UTF1 specific ABC transporters might facilitate adaptation strategies essential for marine environment survival. Thus, the availability of the complete N. seriolae UTF1 genome sequence will provide a valuable resource for comparative genomic studies of N. seriolae isolates, as well as provide new insights into the ecological and functional diversity of the genus Nocardia.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.