Summary The genes required for host‐specific pathogenicity in Fusarium oxysporum can be acquired through horizontal chromosome transfer (HCT). However, it is unknown if HCT commonly contributes to the diversification of pathotypes. Using comparative genomics and pathogenicity phenotyping, we explored the role of HCT in the evolution of F. oxysporum f. sp. fragariae, the cause of Fusarium wilt of strawberry, with isolates from four continents. We observed two distinct syndromes: one included chlorosis (‘yellows‐fragariae’) and the other did not (‘wilt‐fragariae’). All yellows‐fragariae isolates carried a predicted pathogenicity chromosome, ‘chrY‐frag’, that was horizontally transferred at least four times. chrY‐frag was associated with virulence on specific cultivars and encoded predicted effectors that were highly upregulated during infection. chrY‐frag was not present in wilt‐fragariae; isolates causing this syndrome evolved pathogenicity independently. All origins of F. oxysporum f. sp. fragariae occurred outside of the host’s native range. Our data support the conclusion that HCT is widespread in F. oxysporum, but pathogenicity can also evolve independently. The absence of chrY‐frag in wilt‐fragariae suggests that multiple, distinct pathogenicity chromosomes can confer the same host specificity. The wild progenitors of cultivated strawberry (Fragaria × ananassa) did not co‐evolve with this pathogen, yet we discovered several sources of genetic resistance.

Traumatic brain injury (TBI) causes acute and lasting impacts on the brain, driving pathology along anatomical, cellular, and behavioral dimensions. Rodent models offer an opportunity to study the temporal progression of disease from injury to recovery. Transcriptomic and epigenomic analysis were applied to evaluate gene expression in ipsilateral hippocampus at 1 and 14 days after sham ( n = 2 and 4, respectively per time point) and moderate lateral fluid percussion injury ( n = 4 per time point). This enabled the identification of dynamic changes and differential gene expression (differentially expressed genes; DEGs) modules linked to underlying epigenetic response. We observed acute signatures associated with cell death, astrocytosis, and neurotransmission that largely recovered by 2 weeks. Inflammation and immune signatures segregated into upregulated modules with distinct expression trajectories and functions. Whereas most down-regulated genes recovered by 14 days, two modules with delayed and persistent changes were associated with cholesterol metabolism, amyloid beta clearance, and neurodegeneration. Differential expression was paralleled by changes in histone H3 lysine residue 4 trimethylation at the promoters of DEGs at 1 day post-TBI, with the strongest changes observed for inflammation and immune response genes. These results demonstrate how integrated genomics analysis in the pre-clinical setting has the potential to identify stage-specific biomarkers for injury and/or recovery. Though limited in scope here, our general strategy has the potential to capture pathological signatures over time and evaluate treatment efficacy at the systems level.

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Traumatic brain injury (TBI) causes acute and lasting impacts on the brain, driving pathology along anatomical, cellular, and behavioral dimensions. Rodent models offer the opportunity to study TBI in a controlled setting, and enable analysis of the temporal progression that occurs from injury to recovery. We applied transcriptomic and epigenomic analysis, characterize gene expression and in ipsilateral hippocampus at 1 and 14 days following moderate lateral fluid percussion (LFP) injury. This approach enabled us to identify differential gene expression (DEG) modules with distinct expression trajectories across the two time points. The major DEG modules represented genes that were up- or downregulated acutely, but largely recovered by 14 days. As expected, DEG modules with acute upregulation were associated with cell death and astrocytosis. Interestingly, acutely downregulated DEGs related to neurotransmission mostly recovered by two weeks. Upregulated DEG modules related to inflammation were not necessarily elevated acutely, but were strongly upregulated after two weeks. We identified a smaller DEG module with delayed downregulation at 14 days including genes related to cholesterol metabolism and amyloid beta clearance. Finally, differential expression was paralleled by changes in H3K4me3 at the promoters of differentially expressed genes at one day following TBI. Following TBI, changes in cell viability, function and ultimately behavior are dynamic processes. Our results show how transcriptomics in the preclinical setting has the potential to identify biomarkers for injury severity and/or recovery, to identify potential therapeutic targets, and, in the future, to evaluate efficacy of an intervention beyond measures of cell death or spatial learning.

Convergent evolution of phytopathogenicity is poorly described, especially among multiple strains of a single microbial species. We investigated this phenomenon with genetically diverse isolates of Fusarium oxysporum f. sp. fragariae (Fof) that cause one of two syndromes: chlorosis and wilting (the ‘yellows‐fragariae’ pathotype), or only wilting (the ‘wilt‐fragariae’ pathotype). We challenged strawberry (Fragaria × ananassa) plants to root infection by five fungal isolates: three yellows‐fragariae, one wilt‐fragariae and one that is not pathogenic to strawberry. All Fof isolates had chromosome‐level assemblies; three were newly generated. The two pathotypes triggered distinct host responses, especially among phytohormone‐associated genes; yellows‐fragariae isolates strongly induced jasmonic acid‐associated genes, whereas the wilt‐fragariae isolate primarily induced ethylene biosynthesis and signalling. The differentially expressed genes on fungal accessory chromosomes were almost entirely distinct between pathotypes. We identified an ~150 kbp ‘pathogenicity island’ that was horizontally transferred between wilt‐fragariae strains. This predicted pathogenicity island was enriched with differentially expressed genes whose predicted functions were related to plant infection, and only one of these genes was also upregulated in planta by yellows‐fragariae isolates. These results support the conclusion that wilt‐ and yellows‐fragariae cause physiologically distinct syndromes by the expression of discrete repertoires of genes on accessory chromosomes.