Plant pathogenic fungi exhibit significant ecological diversity that is under pressure from climate change, yet their relevance to both human and ecosystem health remains underexplored within the One Health framework. Several phytopathogenic lineages have demonstrated the ability to infect vertebrate hosts. Herein, we introduce the ecological characteristics and genomic plasticity of selected phytopathogenic fungi. Some species adopt generalist lifestyle strategies as endophytes and epiphytes, whereas others develop specialized biotrophic, necrotrophic, or hemibiotrophic modes of infection. Their ecological diversity is facilitated by the horizontal transfer of accessory chromosomes, enabling rapid adaptation and potentially giving rise to new versatile hybrids. Opportunism is defined when traits acquired in a pathogen's preferred niche coincidentally allow survival in other hosts, despite reduced fitness that prevents subsequent transmission. We highlight three filamentous ascomycetes that exemplify ecological versatility and genomic plasticity associated with cross-kingdom opportunistic infections. In Alternaria alternata, melanogenesis and induction of Type 2 inflammation may predispose vulnerable populations to infection. Colletotrichum spp. can cause keratitis and infections in immunocompromised individuals; its pathogenic potential is further supported by melanin production and resistance to dual-use azole antifungals. By contrast, the Fusarium oxysporum species complex demonstrates a broad host range, causing disease in immunocompromised and immunocompetent individuals, with the latter particularly concerning onychomycosis. Its One Health implications are further supported by outbreaks in aquatic vertebrates, the identification of virulence factors implicated in both plant and vertebrate pathogenicity, and resistance to dual-use azole antifungals. Cross-disciplinary and cross-sectoral collaborations should be encouraged to develop mitigation strategies.

Acinetobacter baumannii sequence type 2 (Pasteur ST2), associated with international clone 2, is a major antimicrobial-resistant lineage, but its within-lineage population structure and accessory resistance variation remain incompletely resolved. We analyzed 5612 quality-filtered public genomes from an existing global dataset using PopPUNK, core-genome SNP analysis, AMRFinderPlus, MobileElementFinder and MOB-suite. A dominant PopPUNK cluster contained 5604 genomes (99.86%). Its SNP phylogeny showed dense short-distance relationships within a connected lineage; pairwise distances had a median of 314 SNPs. Four antibiotic classes-beta-lactams, aminoglycosides, phenicols and fosfomycin-were detected in at least 95% of dominant-cluster genomes. The median antibiotic-class annotation hit count was 14 per genome (IQR, 13-15), including intrinsic and lineage-associated determinants. Predicted conjugative and mobilizable plasmid signatures occurred in 52.6% and 42.7% of dominant-cluster genomes, respectively. Across the full cohort, mobile-element and antibiotic-class hit counts were weakly positively correlated (Spearman ρ = 0.191). This unadjusted association was absent among 700 representatives selected one per ≤10-SNP component (ρ = -0.0721; p = 0.0567), and a component-bootstrap interval included zero. Assembly-adjusted associations differed between the full cohort and representatives. The small positive unadjusted collection-year association was not robust to location adjustment and was unsupported in dated representatives. Complete-genome annotations documented both chromosomal and plasmid blaOXA-23 copies and upstream ISAba1 proximity, without establishing promoter activity or resistance phenotype. These findings describe a cohesive ST2 lineage with heterogeneous accessory resistance and plasmid-mobility signatures, while emphasizing the sensitivity of genome-wide associations to assembly characteristics and clonal and geographic sampling.

Fibrillarin is an evolutionarily conserved methyltransferase found in Archaea, algae, yeast, animals, and plants. It catalyzes the 2'-O-methylation (2'-O-Me) of ribosomal RNAs (rRNAs), small nucleolar RNAs (snoRNAs), small nuclear RNAs (snRNAs), and transfer RNAs (tRNAs) as well as the glutamine methylation (Qme) in histone H2A. Fibrillarin interacts with specific accessory proteins and snoRNA guides to perform 2'-O-Me, although it can also act independently in the case of Qme. Additionally, fibrillarin has been reported to exhibit ribonuclease activity and interact with long non-coding RNAs that regulate gene expression. To identify proteins and RNAs that interact with fibrillarin in vivo, we developed a protocol-detailed herein-combining the immunoprecipitation (IP) of a fibrillarin-Yellow Fluorescent Protein (FIB2-YFP) fusion protein in Arabidopsis thaliana with high-sensitivity liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis.

Photobacterium damselae subsp. damselae (PDD), a halophilic, Gram-negative bacterium of the family Vibrionaceae, infects a wide range of aquatic organisms. PDD isolates originating from fish have been characterized in detail, but much less is known about those infecting invertebrates. Currently, only 3 complete PDD genomes isolated from Kuruma shrimp Penaeus (Marsupenaeus) japonicus from Japan are publicly available, severely limiting comparative studies of host adaptation. To address this, we present complete, plasmid-resolved genome assemblies of 4 novel PDD strains (TUMSAT-PD1, -PD2, -PD3, and -PD4) isolated from diseased Kuruma shrimp across multiple prefectures in Japan. Phylogenomic analysis reveals that shrimp PDD strains are genetically heterogeneous and closely related to those infecting other aquatic organisms, suggesting that pathogenicity against shrimp arose independently in multiple PDD strains. While core virulence determinants are chromosomally encoded, we identified key plasmid-borne virulence factors that are likely to enhance the pathogenicity of PDD strains. Comparative analysis with 3 publicly available PDD genomes demonstrated both conserved core virulence determinants and strain-specific accessory genes, reflecting local adaptation and evolutionary diversification. Our findings provide the first geographically expanded genomic framework for Kuruma shrimp-associated PDD, integrating 4 novel Japanese isolates with the existing public genomes. This integrated data set demonstrates that PDD exhibits a generalist evolutionary strategy, capable of rapid adaptation to diverse hosts through conserved virulence machinery and mobile genetic elements. This work significantly expands the genomic basis for understanding PDD epidemiology and pathogenesis within aquaculture systems.

Table olives are among the most important fermented vegetables in the Mediterranean region, with fermentations largely driven by Lactiplantibacillus species. While Lactiplantibacillus pentosus has been extensively studied at the genomic level, genomic information on olive-associated Lactiplantibacillus plantarum remains scarce. To expand current knowledge, three novel L. plantarum strains isolated from table olive fermentations in Spain (Lpl15 and LPT703) and Greece (B282) were subjected to whole-genome sequencing and comparative genomic analysis. Genome assemblies ranged from 3.25 to 3.50 Mb and contained 3,060-3,328 predicted protein-coding genes. While Illumina assemblies remained fragmented, hybrid sequencing produced a complete genome assembly for strain L. plantarum Lpl15, including a complete chromosome and three plasmids. Comparative analyses incorporating L. plantarum genomes from diverse ecological origins, including vegetable fermentations, animal-derived foods, and human-associated environments, were performed using Average Nucleotide Identity (ANI), pangenome analysis, and core-genome phylogeny. Neither ANI nor phylogenomic analyses supported the existence of a distinct lineage associated with table olive fermentations. Functional and metabolic comparisons revealed two major genomic groups linked to ecological origin. Genomes predominantly associated with vegetable fermentations lacked complete nitrogen metabolism pathways, whereas strains of animal origin generally retained these functions. In addition, vegetable-associated strains showed an enrichment of genes involved in exopolysaccharide biosynthesis. Analyses of protein families, domains, and mobilome-related elements further revealed niche-associated genomic patterns. Overall, these results indicate that L. plantarum from table olive fermentations does not constitute a distinct evolutionary lineage. Instead, adaptation appears to be reflected in functional and accessory genomic traits associated with ecological origin, providing new insights into the diversity and adaptive potential of this species across different environments.

Enterobacter cloacae (E. cloacae) is an important healthcare-associated pathogen with increasing antimicrobial resistance. Prophages and phage-inducible chromosomal islands (PICIs) are integral components of the E. cloacae genome, yet their contribution to resistance, virulence, and anti-phage defense remains poorly understood. To address this gap, we analyzed 35 complete E. cloacae genomes, identifying 139 intact prophages (10.8-85.7 kb) with an average GC content (~52%) close to that of the host (54-55%). Most prophages (86.6%) were assigned to the families Peduoviridae and Drexlerviridae within the class Caudoviricetes, and proteome-based clustering showed strong relatedness to phages infecting Enterobacteriaceae. The E. cloacae genomes harbored multiple antimicrobial resistance genes, notably fosA (97%), oqxA/oqxB (89%) and blaCMH-3 (77%). However, on genomic-context verification none were genuinely prophage-encoded; they were instead located on the chromosome or plasmids. Virulence profiling revealed universal presence of ompA and high prevalence of csgG (94%), while the only confirmed prophage-encoded virulence determinants were the Shiga toxin genes stxA and stx1B. Additionally, 16 phage satellites were identified, containing conserved integration, replication, and packaging modules together with diverse accessory and anti-phage defense systems. Overall, prophages and phage satellites drive genome diversification in E. cloacae, with satellites notably serving as reservoirs of anti-phage defense, whereas resistance and virulence genes are located outside prophage and satellite regions.

Meiotic recombination is a multilayered process that shapes genetic diversity while safeguarding genome stability. In mammals, the final distribution of crossovers and non-crossovers emerges from the integration of sequence-specific hotspot specification, chromosome architecture, replication timing, and crossover patterning mechanisms. PRDM9 directs most double-strand break formation to short (typically 1-2 kb), rapidly evolving hotspots by depositing histone marks and remodeling chromatin, whereas in PRDM9-independent contexts, breaks are redirected toward accessible promoters and CpG islands. Yet hotspot marking alone is insufficient: double-strand break formation requires assembly of the SPO11-TOPOVIBL catalytic machinery together with accessory proteins on the chromosome axis, linking recombination initiation to loop-axis organization. Broader regional biases are further imposed by meiotic replication timing, which favors early replicating domains. Downstream, only a small fraction of breaks matures into crossovers through ZMM-dependent stabilization, HEI10/RNF212-mediated dynamics, crossover interference, and the obligate crossover rule. These mechanisms result in sex-specific recombination landscapes, with structural differences in axis length and synapsis dynamics contributing to heterochiasmy. Disruption at any of these control layers can compromise homolog segregation and promote infertility, aneuploidy, recurrent pregnancy loss, or structural genomic disorders. Together, these findings support a hierarchical model in which meiotic recombination is best understood as the integrated output of DNA sequence, chromatin state, chromosome architecture, and choice of repair pathway-based patterning.

Telomeres are specialized chromosomal structures that protect chromosome ends and maintain genome stability. Their organization depends on telomeric DNA repeats, the shelterin complex, accessory factors, and telomerase. While telomere structure and maintenance have been characterized, their dynamics during mammalian mitosis remain incompletely understood. Mitosis involves profound cellular reorganization, including chromatin condensation, spindle formation, and nuclear membrane disassembly and reassembly. Emerging evidence suggests that telomeres participate in these processes and may contribute to proper chromosome segregation and post-mitotic chromatin organization. Studies indicate that telomeric proteins such as TRF1 and TNKS1 interact with centrosomes and spindle components, while telomeres also interface with chromatin and nuclear membrane reassembly factors, including BAF1, LAP2α, and the ESCRT machinery during late mitosis. Defects in these processes or interactions can lead to telomere dysfunction and genomic instability. Understanding telomere dynamics during mitosis is therefore critical for elucidating mechanisms underlying aging, laminopathies, and other telomere-related human diseases.

Stenotrophomonas maltophilia is an emerging multidrug-resistant opportunistic pathogen associated with high morbidity and mortality in hospitalized patients. We present an integrated genomic and phenotypic characterization of 57 clinical S. maltophilia isolates from a tertiary care hospital in Lebanon. Whole-genome sequencing defined resistance profiles, virulence traits, and mobile genetic elements. Multilocus sequence typing revealed marked diversity across 12 known sequence types, with more than half (56%) of isolates assigned to novel or untypable STs. Five ST138 isolates were recovered from respiratory samples in critical care units, a pattern consistent with nosocomial transmission. Phenotypically, 28.1% and 3.5% of isolates were resistant to levofloxacin and trimethoprim-sulfamethoxazole, respectively; 71.9% were non-susceptible to colistin; and one (1.8%) was non-susceptible to minocycline. Trimethoprim-sulfamethoxazole resistance was not associated with sul1 or sul2, and fluoroquinolone resistance was only partially explained by smeD, pointing to multifactorial mechanisms. Virulence genes fliC, smf-1, and katA were broadly conserved, whereas biofilm formation varied markedly. Type I secretion system components hlyB and hlyD occurred in a minority of isolates, with hlyD detected on both chromosomal and plasmid loci in three. A complete type VI secretion system (T6SS) core was identified in four isolates, with VipA subtyping placing most in i4b and a divergent CASM6 variant in i3. Tn3 family transposons linked to metal resistance genes were carried by 17 isolates. Together, these findings reveal a genetically diverse population in which multifactorial resistance, heterogeneous T6SS carriage, variable biofilm capacity, and transposon-linked metal resistance converge to shape clinical adaptability, emphasizing the need for integrated surveillance to guide treatment and infection control.IMPORTANCEStenotrophomonas maltophilia has emerged as an important cause of infections globally. This is largely due to its intrinsic resistance and genomic plasticity. Through integrated genomic and phenotypic characterization of 57 clinical isolates, this study reveals a highly diverse population with a stable core genome and a dynamic accessory genome shaped by mobile genetic elements. The combination of widespread intrinsic resistance, variable acquired resistance traits, and virulence factors highlights the adaptive pathogenic capacity of this organism. These results highlight the importance of combining genomic data with phenotypic analysis to better understand pathogen evolution and transmission. By providing the first comprehensive molecular overview of clinical S. maltophilia isolates from Lebanon, this study supports the implementation of genomic surveillance frameworks and informed infection control strategies to limit the spread of this multidrug-resistant pathogen.

Extended-spectrum β-lactamase genes in foodborne Salmonella enterica can disseminate through mobile multidrug-resistance platforms. IncHI2 plasmids are important resistance vehicles capable of carrying complex resistance regions and facilitating their horizontal transfer across diverse bacterial backgrounds, but the transfer and genomic organization of IncHI2 elements co-carrying blaLAP-2 and blaCTX-M-55 remain insufficiently characterized. This study investigated two multidrug-resistant foodborne isolates recovered in Shanghai in 2022: Salmonella Agona ST13 isolate Sal22C150 and Salmonella Havana ST1527 isolate Sal22P208. Antimicrobial susceptibility testing, whole-genome sequencing, conjugation, plasmid-retention analysis, comparative genomics, as well as strain- and plasmid-level phylogenetic analyses were performed. Both isolates exhibited broad antimicrobial resistance, including resistance to extended-spectrum cephalosporins. In both isolates, blaLAP-2 and blaCTX-M-55 co-transferred with the IncHI2 replicon to Escherichia coli J53 at frequencies of (4.95 ± 0.41) × 10-5 and (4.46 ± 0.42) × 10-6 transconjugants per donor cell, respectively. All tested plasmid markers remained detectable through 20 passages without antimicrobial selection. Complete assembly of Sal22P208 confirmed the location of the three β-lactamase genes on the 275,096 bp IncHI2 plasmid pSal22P208. The plasmid contained a conserved conjugative backbone and mosaic accessory regions carrying 15 antimicrobial-resistance determinants together with mercury- and tellurium-resistance loci. SNP-based analysis placed pSal22P208 within a closely related cluster containing six reference IncHI2 plasmids differing by fewer than 30 SNPs and recovered from Salmonella and E. coli of animal, food, and human origin, suggesting a broad distribution of this plasmid lineage across diverse bacterial and ecological backgrounds. Sal22P208 additionally contained a Tn3-associated chromosomal multidrug-resistance region between rpmJ and rpmE that shared extensive structural similarity with a region in Citrobacter braakii LBA3. These findings highlight the role of transferable IncHI2 resistance platforms in the horizontal dissemination and short-term post-transfer maintenance of linked resistance determinants, while chromosomally integrated resistance regions may provide an additional route for the accumulation and inheritance of multidrug resistance in foodborne Salmonella.

Salmonella poses a significant threat to human and animal health. However, the relationship among population diversity, antibiotic resistance, and infection risk remains largely unexplored. In this study, 69 Salmonella strains were isolated from diseased poultry in Jiangxi Province from 2021 to 2024. Using whole-genome sequencing, serotype prediction, MLST, virulence and resistance gene analysis, antibiotic susceptibility testing, and mobile genetic element annotation, we characterized the diversity, resistance profiles, and transmission mechanisms of these strains. The results showed high diversity, with Salmonella enterica subsp. enterica serovar Typhimurium (>60%) and ST19 (62.31%) as the dominant serovar and sequence type, respectively. Several avian isolates were genomically similar to human isolates, indicating potential zoonotic risk. All strains harbored conserved core virulence modules, whereas accessory modules (e.g., cdtB, astA, pefA) varied and may affect pathogenicity. The multidrug resistance rate was 97.1%, with 100% resistance to erythromycin, tilmicosin and tiamulin, and resistance rates of 91.3%, 84.1%, and 71.0% to sulfonamides, enrofloxacin, and ceftiofur, respectively. Sixty-eight resistance genes were identified. Highly conserved antimicrobial resistance gene (ARG) modules (e.g., sul2-aph(3″)-Ib-aph(6')-Id-tet(A)) were shared between chromosomes and plasmids and were flanked by mobile elements such as Tn3 and IS3. Genomic islands (GIs) and plasmids in some strains carried resistance gene clusters highly homologous to those in pathogens from humans, pigs, and chickens, suggesting active horizontal transfer of resistance genes across hosts. This study revealed high diversity, prevalent multidrug resistance, and active horizontal transfer of resistance genes in avian-derived Salmonella from Jiangxi Province, emphasizing the need for cross-host resistance monitoring and antibiotic management within the 'One Health' framework.

Fusarium oxysporum isolates causing Fusarium wilt in mitsuba (Cryptotaenia japonica Hassk.; also referred to as Japanese honeywort, Japanese honewort, or Japanese parsley) have traditionally been classified as f. sp. apii. However, some reports have indicated that the host-pathogenic F. oxysporum isolates derived from mitsuba are nonpathogenic to celery, the principal host of f. sp. apii. In this study, we aimed to elucidate the differences among isolates from mitsuba, coriander, and celery in terms of host range, phylogenetic relationships, genomic synteny, and effector profiles. Inoculation assays revealed a clear distinction in host range between the mitsuba, coriander, and celery isolates. Phylogenetic analyses based on the rDNA intergenic spacer and translation elongation factor sequences indicated a distant relationship between mitsuba isolates and those from coriander and celery. Whole-genome analysis based on high-quality de novo-assembled genomes, including telomere-to-telomere-level assemblies of isolates from mitsuba, coriander, and celery, showed that the mitsuba isolates possess conserved accessory chromosomal regions absent in celery and coriander isolates. Moreover, effector profiling identified a specific pattern of effector repertoires shared by the mitsuba isolates. These findings suggest that the host-pathogenic F. oxysporum isolates derived from mitsuba represent a forma specialis distinct from f. sp. apii. Thus, we propose designating the F. oxysporum isolates from mitsuba that cause Fusarium wilt as Fusarium oxysporum f. sp. crypti forma specialis nova.