Gut pathobiome mediates behavioral and developmental disorders in biotoxin-exposed amphibians.

Emerging evidence suggests a link between alterations in the gut microbiome and adverse health outcomes in the hosts exposed to environmental pollutants. Yet, the causal relationships and underlying mechanisms remain largely undefined. Here we show that exposure to biotoxins can affect gut pathobiome assembly in amphibians, which in turn triggers the toxicity of exogenous pollutants. We used Xenopus laevis as a model in this study. Tadpoles exposed to tropolone demonstrated notable developmental impairments and increased locomotor activity, with a reduction in total length by 4.37%-22.48% and an increase in swimming speed by 49.96%-84.83%. Fusobacterium and Cetobacterium are predominant taxa in the gut pathobiome of tropolone-exposed tadpoles. The tropolone-induced developmental and behavioral disorders in the host were mediated by assembly of the gut pathobiome, leading to transcriptome reprogramming. This study not only advances our understanding of the intricate interactions between environmental pollutants, the gut pathobiome, and host health but also emphasizes the potential of the gut pathobiome in mediating the toxicological effects of environmental contaminants.

Phyllosphere microbiome induces host metabolic defence against rice false-smut disease.

Mutualistic interactions between host plants and their microbiota have the potential to provide disease resistance. Most research has focused on the rhizosphere, but it is unclear how the microbiome associated with the aerial surface of plants protects against infection. Here we identify a metabolic defence underlying the mutualistic interaction between the panicle and the resident microbiota in rice to defend against a globally prevalent phytopathogen, Ustilaginoidea virens, which causes false-smut disease. Analysis of the 16S ribosomal RNA gene and internal transcribed spacer sequencing data identified keystone microbial taxa enriched in the disease-suppressive panicle, in particular Lactobacillus spp. and Aspergillus spp. Integration of these data with primary metabolism profiling, host genome editing and microbial isolate transplantation experiments revealed that plants with these taxa could resist U. virens infection in a host branched-chain amino acid (BCAA)-dependent manner. Leucine, a predominant BCAA, suppressed U. virens pathogenicity by inducing apoptosis-like cell death through H2O2 overproduction. Additionally, preliminary field experiments showed that leucine could be used in combination with chemical fungicides with a 50% reduction in dose but similar efficacy to higher fungicide concentrations. These findings may facilitate protection of crops from panicle diseases prevalent at a global scale.

Plant pathogenesis: Toward multidimensional understanding of the microbiome.

Single pathogen-targeted disease management measure has shown drawbacks in field efficacy under the scenario of global change. An in-depth understanding of plant pathogenesis will provide a promising solution but faces the challenges of the emerging paradigm involving the plant microbiome. While the beneficial impact of the plant microbiome is well characterized, their potential role in facilitating pathological processes has so far remained largely overlooked. To address these unsolved controversies and emerging challenges, we hereby highlight the pathobiome, the disease-assisting portion hidden in the plant microbiome, in the plant pathogenesis paradigm. We review the detrimental actions mediated by the pathobiome at multiple scales and further discuss how natural and human triggers result in the prevalence of the plant pathobiome, which would probably provide a clue to the mitigation of plant disease epidemics. Collectively, the article would advance the current insight into plant pathogenesis and also pave a new way to cope with the upward trends of plant disease by designing the pathobiome-targeted measure.

Mechanism of Fusarium graminearum Resistance to Ergosterol Biosynthesis Inhibitors: G443S Substitution of the Drug Target FgCYP51A.

Fusarium head blight (FHB), caused by the Fusarium graminearum species complex, is a devastating fungal disease resulting in substantial yield and quality losses. Ergosterol biosynthesis inhibitors (EBIs) are the most popular chemicals for controlling FHB. Recently, the resistance of F. graminearum to EBIs has emerged in the field, and an amino acid substitution (G443S) of the sterol 14α-demethylase FgCYP51A was detected in the field resistant strains. To further illustrate the resistance mechanism of F. graminearum to EBIs, site-directed mutants conferring the G443S substitution of FgCYP51A were generated from the progenitor strain PH-1 via genetic transformation with site-directed mutagenesis. We found that the FgCYP51A-G443S substitution significantly decreased the sensitivity of F. graminearum to EBIs with EC50 values ranging from 0.1190 to 0.2302 µg mL-1 and EC90 values ranging from 1.3420 to 9.1119 µg mL-1 for tebuconazole. Furthermore, the FgCYP51A-G443S substitution decreased sexual reproduction and virulence, which will reduce the initial infection source of pathogen populations in the field, while the increase of sporulation capability may enhance the frequencies of the disease cycle, thereby contributing to epidemics of FHB disease. Surprisingly, the FgCYP51A-G443S substitution accelerated DON biosynthesis by upregulating TRI5 expression and enhancing the fluorescence intensity of TRI1-GFP, the marker protein of Fusarium toxisomes. Thus, we concluded that the FgCYP51A-G443S substitution regulates EBI-fungicide resistance and DON biosynthesis, increasing the risk of fungicide resistance development in the field, thereby threatening the control efficacy of EBIs against FHB.

Keystone taxa-mediated bacteriome response shapes the resilience of the paddy ecosystem to fungicide triadimefon contamination.

The increasing input of fungicides has emerged as a global concern for agroecosystem stability and sustainability. Agroecosystem resilience has been linked to microbiome response, however, is not well understood. Focusing on a widespread triazole-class fungicide triadimefon in the paddy ecosystem, we characterized that the soils and sediments were dominant triadimefon reservoirs with the peak level at 195 µg kg-1 and 31.3 µg kg-1, respectively, but essential for the resilience of paddy ecosystem to triadimefon. In paddy simulation models, the half-life of triadimefon in soil-sediment was 8.4-28.9 days, while it was prolonged to 86.6-115.5 days after elimination of resident microbial community. Phospholipid fatty acid profiling and high-throughput sequencing showed that the distinctive bacterial community responses contributed to variable degradation of triadimefon in paddy soils and sediments. Sphingomonas and Xanthomonas were identified as positive responders of the keystone taxa in the responsive bacteriome, whereas Enterobacter were negative responders that declined over time. Synthetic assemblages combined with quantitative polymerase chain reaction further validated that Sphingomonas and Xanthomonas were involved in sustaining soil-sediment resilience to triadimefon contamination. Collectively, our results revealed that the shaping of soil and sediment bacteriomes was responsible for the resilience of the paddy agroecosystem to fungicide contamination.

Antifungal Activity of Quinofumelin against Fusarium graminearum and Its Inhibitory Effect on DON Biosynthesis.

Fusarium graminearum, causal agent of Fusarium head blight (FHB), causes a huge economic loss. No information is available on the activity of quinofumelin, a novel quinoline fungicide, against F. graminearum or other phytopathogens. In this study, we used mycelial growth and spore germination inhibition methods to determine the inhibitory effect of quinofumelin against F. graminearum in vitro. The results indicated that quinofumelin excellently inhibited mycelial growth and spore germination of F. graminearum, with the average EC50 values of 0.019 ± 0.007 µg/mL and 0.087 ± 0.024 µg/mL, respectively. In addition, we found that quinofumelin could significantly decrease deoxynivalenol (DON) production and inhibit the expression of DON-related gene TRI5 in F. graminearum. Furthermore, we found that quinofumelin could disrupt the formation of Fusarium toxisome, a structure for producing DON. Western blot analysis demonstrated that the translation level of TRI1, a marker gene for Fusarium toxisome, was suppressed by quinofumelin. The protective and curative assays indicated that quinofumelin had an excellent control efficiency against F. graminearum on wheat coleoptiles. Taken together, quinofumelin exhibits not only an excellent antifungal activity on mycelial growth and spore germination, but also could inhibit DON biosynthesis in F. graminearum. The findings provide a novel candidate for controlling FHB caused by F. graminearum.

Antifungal Activity and Biological Characteristics of the Novel Fungicide Quinofumelin Against Sclerotinia sclerotiorum.

Sclerotinia sclerotiorum is a devastating plant pathogen with a broad host range and worldwide distribution. The application of chemical fungicides is a primary strategy for controlling this pathogen. However, under the high selective pressure of chemical fungicides, fungicide resistance has emerged and gradually increased, resulting in the failure to control S. sclerotiorum in the field. Quinofumelin is a novel quinoline fungicide, but its antifungal activities against plant pathogens have been rarely reported. Here, we determined the antifungal activity of quinofumelin against S. sclerotiorum in vitro and in planta. The median effect concentration (EC50) values ranged from 0.0004 to 0.0059 µg ml-1 with a mean EC50 of 0.0017 ± 0.0009 µg ml-1 and were normally distributed (P = 0.402). In addition, no cross resistance was observed between quinofumelin and other fungicides, dimethachlone, boscalid, or carbendazim, which are commonly used to manage S. sclerotiorum. Quinofumelin did not affect glycerol and oxalic acid production of either carbendazim-sensitive or -resistant isolates. Moreover, quinofumelin exhibited excellent protective, curative, and translaminar activity against S. sclerotiorum on oilseed rape leaves. Protective activity was higher than curative activity. Interestingly, quinofumelin inhibited the formation of the infection cushion in S. sclerotiorum, which may contribute to the control efficacy of quinofumelin against S. sclerotiorum in the field. Our findings indicate that quinofumelin has excellent control efficacy against S. sclerotiorum in vitro and in planta as compared with extensively used fungicides and could be used to manage carbendazim- and dimethachlone-resistance in S. sclerotiorum in the field.