Enterobacter cloacae is a bacterium that can prevent seedling damping-off by Globisporangium ultimum (formerly Pythium ultimum ). This bacterium suppresses damping-off by metabolizing the fatty acid cue released by germinating seeds that initiates G. ultimum sporangia germination and infection. However, this suppression mechanism has been unreliable because it only occurs only when carbohydrates are scarce. We hypothesized that niche preemption by competitor bacteria in carbohydrate rich environments could enhance the pathogen suppression success by E. cloacae by narrowing its realized niche to consist mainly of fatty acids. We tested this hypothesis through pair-wise competition experiments between E. cloacae and bacteria with varying niche overlap profiles and measured the germination of G. ultimum sporangia. After these trials, we postulated that other chemical substrates may influence the behavior of G. ultimum and E. cloacae based on patterns witnessed; namely amygdalin, hydroxybenzoic acid, palatinose, D-gluconic acid, and L-glutamic acid. We then exposed G. ultimum and E. cloacae to these compounds to determine how they influenced the suppression behavior of E. cloacae and the germination of G. ultimum sporangia. We found that although niche preemption does not predict pathogen suppression patterns between E. cloacae and competitor bacteria, niche overlap was inversely correlated with sporangia germination for gram-negative bacteria; the opposite pattern predicted by niche overlap. We also found several taxa that significantly enhanced the pathogen suppression by E. cloacae . Finally, we found that amygdalin and 4-hydroxybenzoic acid inhibited the suppression performance E. cloacae and found that 4-hydroxybenzoic acid, palatinose, and L-glutamic acid inhibited sporangia germination.
Wheat head blast is a major threat to wheat in South America, but epidemics vary across space and time because they depend on seasonal weather. In subtropical and temperate regions, epidemics occur only when winter conditions allow inoculum survival and weather during heading favors infection. As a result, epidemiological data from these regions remain limited. In 2023, unusual weather led to widespread disease occurrence across parts of southern South America. In this study, we adopted a climate-analog framework to define the climatic fingerprint of the 2023 epidemic season and assess whether similar conditions occurred historically (1992-2023) or recur under mid-century climate projections (2024-2055). Two biologically informed indices were developed for each year: winter thermal favorability, representing conditions for inoculum carryover, and hygrothermal suitability during heading. Historical years were compared with 2023 conditions at each site and with the 2023 Passo Fundo epidemic. Analog years were rare in the historical recor, confirming the exceptional nature of 2023. Future projections did not show a uniform increase in exact 2023 analogs; the clearest increases occurred under RCP2.6 at Santa Rosa (BR), Passo Fundo (BR), and Pergamino (AR). In contrast, years jointly exceeding both benchmark indices increased at every site in the within-site analysis and generally increased more under RCP8.5. In the cross-site analysis, only Brazilian sites reproduced or frequently exceeded the Passo Fundo benchmark, whereas the Argentine sites remained climatically distinct. Climate change projections therefore shifted conditions beyond the 2023 benchmarks more consistently than it increased the recurrence of years closely resembling 2023.
Fhb7 is a gene derived from the homoeologous group-7 chromosomes of tall wheatgrass ( Thinopyrum species), which confers resistance to Fusarium head blight (FHB) in wheat. Two resistance alleles at the Fhb7 locus ( Fhb7 Thp and Fhb7 The2) were identified from Th. ponticum and Th. elongatum , respectively, and introgressed into the wheat genome by homoeologous recombination. Fhb7 Thp was first cloned and reported to encode a glutathione S-transferase (GST), which detoxifies trichothecenes through de-epoxidation. However, a recent study has questioned the role of GST in Fhb7 -mediated FHB resistance. To decipher the function of two GST-encoding alleles, Fhb7 Thp and Fhb7 The2, in FHB resistance, we generated haploid plants from three spring wheat lines (CS-Fhb7, WGC002, and FW23-009-80) carrying Fhb7 Thp or Fhb7 The2 through wide hybridizations with transgenic maize expressing Cas9 and guide RNA ( gRNA ) targeting GST . Of 57, 35, and 74 haploid plants derived from CS-Fhb7, WGC002, and FW23-009-80, respectively, 16, 5, and 9 had an insertion/deletion at the target sites of GST . Greenhouse evaluation of doubled haploid (DH) lines derived from the haploid plants for FHB resistance indicated that the GST -edited DH lines were significantly more susceptible and accumulated more deoxynivalenol (DON) than their corresponding wildtypes and non-edited DH lines, confirming GST as the causal gene for Fhb7 -mediated FHB resistance. This study also demonstrated the power of wheat × maize hybridization coupled with genome editing in validating gene function in wheat.
The American beech (Fagaceae: Fagus grandifolia ) is a mast-bearing canopy tree species that plays a vital role in northeastern North American forest ecosystems. Beech leaf disease (BLD) is a newly emergent and fast-moving forest disease affecting millions of American beech trees. As the disease advances, there is a significant reduction of bud and leaf survival, leading to defoliation, reduction of the canopy, and eventually tree mortality. The causal agent, the foliar nematode Litylenchus crenatae (Lc), is regarded as a new invasive species with potential origins in Asia. In addition to its association with beech buds and foliage, this nematode may also exploit senescent leaves as a stable reservoir of inoculum on the forest floor. This study investigates a potential role for infected beech leaf litter in the spread of BLD by quantifying extracted nematode individuals, observing their survival in desiccated leaves over one annual cycle, and exploring environmental predictors that may be associated with their survival. In one northeastern forest, the leaf litter around 15 symptomatic trees were monitored. Living Lc were consistently extracted from leaf litter in every month sampled, and collection of viable nematodes persisted up to 14 weeks in desiccated leaf tissues. Predicted nematode survival was not significantly influenced by prior month’s precipitation, but both vapor pressure deficit and freeze-thaw cycles were correlated with Lc survival after desiccation. These findings identify infected beech leaf litter as a plausible environmental reservoir of viable Lc and suggest that natural desiccation process may not reliably eliminate the inoculum.
Soybean sudden death syndrome (SDS), caused by Fusarium virguliforme , is a major constraint to soybean ( Glycine max ) production in North America, yet disease expression and yield loss remain highly variable across environments. From 2017 to 2024, field trials were conducted across 66 site-years in Michigan to evaluate the relative contributions of pathogen pressure, edaphic factors, and management inputs to SDS development and soybean yield. Fusarium virguliforme DNA abundance and soybean cyst nematode (SCN; Heterodera glycines ) density were quantified, alongside soil properties, root disease index (RDX), foliar disease index (FDX), and yield, using linear mixed models and multivariate analyses. Across site-years, F. virguliforme DNA abundance and SCN density were consistent predictors of both FDX and yield, while soil pH was significantly associated with pathogen abundance, disease expression, and yield. However, FDX itself was not consistently aligned with yield loss, and substantial yield reductions were observed in the absence of visible foliar symptoms. Significant seed treatment effects were not detected across all site-years but were detected among site-years under high disease pressure, with yield and revenue benefits confined to site-years characterized by elevated pathogen pressure. Similarly, cultivar SDS tolerance reduced disease and protected yield under specific conditions but was not consistently effective across environments. These results demonstrate that SDS is best understood as a context-dependent disease complex structured by interacting soilborne pathogens and environmental gradients, with management inputs exerting secondary, conditional effects. Collectively, these findings support diagnostic-informed, risk-stratified strategies for integrated SDS management.
