UDP-glucosyltransferase HvUGT13248 confers type II resistance to Fusarium graminearum in barley.

Fusarium head blight (FHB) of barley (Hordeum vulgare) causes yield losses and accumulation of trichothecene mycotoxins (e.g. deoxynivalenol [DON]) in grains. Glucosylation of DON to the nontoxic DON-3-O-glucoside (D3G) is catalyzed by UDP-glucosyltransferases (UGTs), such as barley UGT13248. We explored the natural diversity of UGT13248 in 496 barley accessions and showed that all carried potential functional alleles of UGT13248, as no genotypes showed strongly increased seedling sensitivity to DON. From a TILLING population, we identified 2 mutant alleles (T368I and H369Y) that, based on protein modeling, likely affect the UDP-glucose binding of UGT13248. In DON feeding experiments, DON-to-D3G conversion was strongly reduced in spikes of these mutants compared to controls, and plants overexpressing UGT13248 showed increased resistance to DON and increased DON-to-D3G conversion. Moreover, field-grown plants carrying the T368I or H369Y mutations inoculated with Fusarium graminearum showed increased FHB disease severity and reduced D3G production. Barley is generally considered to have type II resistance that limits the spread of F. graminearum from the infected spikelet to adjacent spikelets. Point inoculation experiments with F. graminearum showed increased infection spread in T368I and H369Y across the spike compared to wild type, while overexpression plants showed decreased spread of FHB symptoms. Confocal microscopy revealed that F. graminearum spread to distant rachis nodes in T368I and H369Y mutants but was arrested at the rachis node of the inoculated spikelet in wild-type plants. Taken together, our data reveal that UGT13248 confers type II resistance to FHB in barley via conjugation of DON to D3G.

Catalytic Properties of [PSiP] Pincer Cobalt(II) Chlorides Supported by Trimethylphosphine for Alkene Hydrosilylation Reactions.

In this paper, six silyl [PSiP] pincer cobalt(II) chlorides 1-6 [(2-Ph2PC6H4)2MeSiCo(Cl)(PMe3)] (1), [(2-Ph2PC6H4)2HSiCo(Cl)(PMe3)] (2), [(2-Ph2PC6H4)2PhSiCo(Cl)(PMe3)] (3), [(2-iPr2PC6H4)2HSiCo(Cl)(PMe3)] (4), [(2-iPr2PC6H4)2MeSiCo(Cl)(PMe3)] (5), and [(2-iPr2PC6H4)2PhSiCo(Cl)(PMe3)] (6)) were prepared from the corresponding [PSiP] pincer preligands (L1-L6), CoCl2 and PMe3 by Si-H bond activation. The catalytic activity of complexes 1-6 for alkene hyrdosilylation was studied. It was confirmed that complex 1 is the best catalyst with excellent regioselectivity among the six complexes. Using 1 as the catalyst, the catalytic reaction was completed within 1 h at 50 °C, predominantly affording Markovnikov products for aryl alkenes and anti-Markovnikov products for aliphatic alkene substrates. During the investigation of the catalytic mechanism, the Co(II) hydrides [(2-Ph2PC6H4)2MeSiCo(H)(PMe3)] (8) and [(2-iPr2PC6H4)2MeSiCo(H)(PMe3)] (9) were obtained from the stoichiometric reactions of complex 1 and 5 with NaBHEt3, respectively. Complexes 8 and 9 could also be obtained by the reactions of preligands L1 and L5 with Co(PMe3)4 via Si-H bond cleavage. More experiments corroborated that complex 8 is the real catalyst for this catalytic system. Under the same catalytic conditions as complex 1, using complex 8 as a catalyst, complete conversion of styrene was also achieved in 1 h, and the selectivity remained unchanged. Based on the experimental results, we propose a plausible mechanism for this catalytic reaction. The addition of B(C6F5)3 to catalyst 1 can reverse the selectivity of styrene hydrosilylation from the Markovnikov product as the main product (b/l = 99:1) to the anti-Markovnikov product as the main product (b/l = 40:60). Further study indicated that using the (CoCl2 + L1) system instead of complex 1, the selectivity was changed from Markovnikov to anti-Markovnikov product (b/l = 1:99.7). Therefore, the selectivity for the substrate styrene is influenced by the presence of a PMe3 ligand. The different selectivities may be caused by different active species. For the system of complex 1, a cobalt(II) hydride is the real catalyst, but for the (CoCl2 + L1) system, a cobalt(I) complex is proposed as active species. The molecular structures of Co(II) compounds 5 and 9 were resolved by single-crystal X-ray diffraction.

Effect of Quantitative Wheat Resistance on the Aggressiveness of Fusarium graminearum.

Little is known about the selection pressures acting on plant pathogen populations, especially those applied by quantitative forms of resistance. Fusarium graminearum causes Fusarium head blight in wheat, producing significant yield losses and mycotoxin contamination. Quantitative host resistance is the best method to control Fusarium head blight. However, there needs to be more understanding of how disease resistance affects the evolution of plant pathogens. The aim of this study was to determine if the presence or absence of wheat resistance influenced the fitness components and genomic regions of F. graminearum. Thirty-one isolates from highly susceptible and 25 isolates from moderately resistant wheat lines were used. Isolate aggressiveness was measured by the area under the disease progress curve, visually damaged kernels, and deoxynivalenol contamination. The in vitro growth rate and spore production were also measured. Two whole-genome scans for selection were conducted with 333,297 single-nucleotide polymorphisms. One scan looked for signatures of selection in the entire sample, and the other scan was for divergent selection between the isolates from moderately resistant wheat and highly susceptible wheat. The subsample of isolates from highly susceptible wheat was primarily aggressive. Several regions of the F. graminearum genome with signatures for selection were identified. The moderately resistant wheat varieties used in this study did not select more aggressive isolates, suggesting that quantitative resistance is a durable method to control Fusarium head blight.

A Glutathione S-Transferase from Thinopyrum ponticum Confers Fhb7 Resistance to Fusarium Head Blight in Wheat.

Fusarium head blight (FHB), mainly incited by Fusarium graminearum, has caused great losses in grain yield and quality of wheat globally. Fhb7, a major gene from 7E chromosome of Thinopyrum ponticum, confers broad resistance to multiple Fusarium species in wheat and has recently been cloned and identified as encoding a glutathione S-transferase (GST). However, some recent reports raised doubt about whether GST is the causal gene of Fhb7. To resolve the discrepancy and validate the gene function of GST in wheat, we phenotyped Fhb7 near-isogenic lines (Jimai22-Fhb7 versus Jimai22) and GST overexpressed lines for FHB resistance. Jimai22-Fhb7 showed significantly higher FHB resistance with a lower percentage of symptomatic spikelets, Fusarium-damaged kernels, and deoxynivalenol content than susceptible Jimai22 in three experiments. All the positive GST transgenic lines driven by either the maize ubiquitin promoter or its native promoter with high gene expression in the wheat cultivar 'Fielder' showed high FHB resistance. Only one maize ubiquitin promoter-driven transgenic line showed low GST expression and similar susceptibility to Fielder, suggesting that high GST expression confers Fhb7 resistance to FHB. Knockout of GST in the Jimai22-Fhb7 line using CRISPR-Cas9-based gene editing showed significantly higher FHB susceptibility compared with the nonedited control plants. Therefore, we confirmed GST as the causal gene of Fhb7 for FHB resistance. Considering its major effect on FHB resistance, pyramiding Fhb7 with other quantitative trait loci has a great potential to create highly FHB-resistant wheat cultivars.

Mechanisms of Cardiovascular Toxicities Induced by Cancer Therapies and Promising Biomarkers for Their Prediction: A Scoping Review.

AIM: With the advancement of anti-cancer medicine, cardiovascular toxicities due to cancer therapies are common in oncology patients, resulting in increased mortality and economic burden. Cardiovascular toxicities caused by cancer therapies include different severities of cardiomyopathy, arrhythmia, myocardial ischaemia, hypertension, and thrombosis, which may lead to left ventricular dysfunction and heart failure. This scoping review aimed to summarise the mechanisms of cardiovascular toxicities following various anti-cancer treatments and potential predictive biomarkers for early detection. METHODS: PubMed, Cochrane, Embase, Web of Science, Scopus, and CINAHL databases were searched for original studies written in English related to the mechanisms of cardiovascular toxicity induced by anti-cancer therapies, including chemotherapy, targeted therapy, immunotherapy, radiation therapy, and relevant biomarkers. The search and title/abstract screening were conducted independently by two reviewers, and the final analysed full texts achieved the consensus of the two reviewers. RESULTS: A total of 240 studies were identified based on their titles and abstracts. In total, 107 full-text articles were included in the analysis. Cardiomyocyte and endothelial cell apoptosis caused by oxidative stress injury, activation of cell apoptosis, blocking of normal cardiovascular protection signalling pathways, overactivation of immune cells, and myocardial remodelling were the main mechanisms. Promising biomarkers for anti-cancer therapies related to cardiovascular toxicity included placental growth factor, microRNAs, galectin-3, and myeloperoxidase for the early detection of cardiovascular toxicity. CONCLUSION: Understanding the mechanisms of cardiovascular toxicity following various anti-cancer treatments could provide implications for future personalised treatment methods to protect cardiovascular function. Furthermore, specific early sensitive and stable biomarkers of cardiovascular system damage need to be identified to predict reversible damage to the cardiovascular system and improve the effects of anti-cancer agents.

Path analysis of self-care amongst community-dwelling pre-ageing and older adults with chronic diseases: A salutogenic model.

With the trend towards ageing population globally, the salutogenic model can be integrated in interventions for pre-ageing and older adults to better support healthy ageing. However, there is limited research examining the salutogenic model's pathway amongst pre-ageing and older adults. Hence, this study aims to investigate pathways of the salutogenic model amongst pre-ageing and older adults with chronic diseases. Two hundred and eight pre-ageing and older adults were recruited from 11 Senior Activity Centres in Singapore. Data was collected using a self-reported questionnaire and analysed using path analyses. The indirect pathway from Subjective Cognitive Complaints to self-care abilities via sense of coherence and health practices were significant. Participants with higher sense of coherence may have increased capacities to execute more complex forms of self-care. Future interventions integrating the salutogenic model could enhance pre-ageing and older adults' self-care abilities to cope with chronic diseases and contribute to healthy ageing.

The Fusarium graminearum Transporters Abc1 and Abc6 Are Important for Xenobiotic Resistance, Trichothecene Accumulation, and Virulence to Wheat.

The plant pathogenic fungus Fusarium graminearum is the causal agent of Fusarium head blight (FHB) disease on small-grain cereals. F. graminearum produces trichothecene mycotoxins such as deoxynivalenol (DON) that are required for full virulence. DON must be exported outside the cell to cause FHB disease, a process that may require the involvement of membrane-bound transporters. In this study, we show that the deletion of membrane-bound transporters results in reduced DON accumulation as well as reduced FHB symptoms on wheat. Deletion of the ATP-binding cassette (ABC) transporter gene Abc1 results in the greatest reduction in DON accumulation and virulence. Deletion of another ABC transporter gene, Abc6, also reduces FHB symptoms to a lesser degree. Combining deletions fails to reduce DON accumulation or virulence in an additive fashion, even when a ∆abc1 deletion is included. Heterologous expression of F. graminearum transporters in a DON-sensitive strain of yeast confirms Abc1 as a major DON resistance mechanism; furthermore, it suggests that Abc1 is directly participating in DON transport rather than facilitating DON transport though other means. Yeast expression further indicates that multiple transporters, including Abc1, play an important role in resistance to the wheat phytoalexin 2-benzoxazolinone (BOA) and other xenobiotics. Thus, Abc1 may contribute to virulence on wheat both by facilitating export of DON and by providing resistance to the wheat phytoalexin BOA. This research provides useful information that may aid in designing novel management techniques of FHB or other destructive plant diseases.

Optimal Timing of Fungicide Application to Manage Fusarium Head Blight in Winter Barley.

Fusarium head blight (FHB) is among the chief threats to profitable barley production, and fungicide applications are one of two main strategies for reducing FHB damage to barley crops. However, there is very little published information on optimal timing of such applications. A 4-year field study was conducted with winter barley in Raleigh, North Carolina, to compare three timings for fungicide application: 50% spike emergence (Zadoks growth stage or GS 55), 100% spike emergence (GS 59), and 6 days after GS 59. Three winter barley cultivars with varying levels of FHB resistance were grown for four successive years (2018 to 2021) in a split-plot experiment and inoculated each spring with Fusarium-infected corn spawn. Three fungicides were compared: propiconazole + pydiflumetofen (Miravis Ace), prothioconazole + tebuconazole (Prosaro), and metconazole (Caramba). Correlations among visual symptoms and assays of harvested grain were modest and were weakened by fungicide applications. Across years and cultivars, deoxynivalenol (DON) and percent Fusarium-infected kernels were most reduced relative to the nontreated control by fungicide applications at the latest timing (GS 59 + 6 days). The early (GS 55) timing resulted in DON not significantly different from the nontreated control. Based on these results, it is recommended that to minimize damage from FHB, fungicide should be applied to winter barley several days after GS 59 (100% spike emergence), and not before GS 59.

Non-native plant invasion can accelerate global climate change by increasing wetland methane and terrestrial nitrous oxide emissions.

Approximately 17% of the land worldwide is considered highly vulnerable to non-native plant invasion, which can dramatically alter nutrient cycles and influence greenhouse gas (GHG) emissions in terrestrial and wetland ecosystems. However, a systematic investigation of the impact of non-native plant invasion on GHG dynamics at a global scale has not yet been conducted, making it impossible to predict the exact biological feedback of non-native plant invasion to global climate change. Here, we compiled 273 paired observational cases from 94 peer-reviewed articles to evaluate the effects of plant invasion on GHG emissions and to identify the associated key drivers. Non-native plant invasion significantly increased methane (CH4 ) emissions from 129 kg CH4 ha-1  year-1 in natural wetlands to 217 kg CH4 ha-1  year-1 in invaded wetlands. Plant invasion showed a significant tendency to increase CH4 uptakes from 2.95 to 3.64 kg CH4 ha-1  year-1 in terrestrial ecosystems. Invasive plant species also significantly increased nitrous oxide (N2 O) emissions in grasslands from an average of 0.76 kg N2 O ha-1  year-1 in native sites to 1.35 kg N2 O ha-1  year-1 but did not affect N2 O emissions in forests or wetlands. Soil organic carbon, mean annual air temperature (MAT), and nitrogenous deposition (N_DEP) were the key factors responsible for the changes in wetland CH4 emissions due to plant invasion. The responses of terrestrial CH4 uptake rates to plant invasion were mainly driven by MAT, soil NH4 + , and soil moisture. Soil NO3 - , mean annual precipitation, and N_DEP affected terrestrial N2 O emissions in response to plant invasion. Our meta-analysis not only sheds light on the stimulatory effects of plant invasion on GHG emissions from wetland and terrestrial ecosystems but also improves our current understanding of the mechanisms underlying the responses of GHG emissions to plant invasion.

Past Exposure to Cigarette Smoke Aggravates Cognitive Impairment in a Rat Model of Vascular Dementia via Neuroinflammation.

Smoking is a risk factor for dementia. Cognitive function can be partially restored after quitting smoking, but still lower than never smoked group. The underlying mechanisms still remain unclear. The effects of smoking cessation combined with cerebral chronic hypoperfusion (CCH) on cognitive function have never been described. Here, we established a cigarette smoking cessation model, a CCH model, and a cigarette smoking cessation plus CCH model. We investigated cognitive function in these models and the mechanisms of the neuroinflammation, nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3(NLRP3)/cysteine aspartate-specific proteinase (caspase-1)/interleukin- 1ß (IL-1ß) pathway, and eucaryotic initiation factor 2α (eIF2α) /autophagy pathway. We used morris water maze (MWM) and novel object recognition (NOR) test to evaluate cognitive function in rats. Nissl staining was performed to observe cell morphology in the hippocampal CA1 area. A neuroinflammatory marker (glial fibrillary acidic protein, GFAP) was assessed by Western blot analysis and immunohistochemistry staining. IL-1ß levels were detected by ELISA. The protein levels of NLRP3/caspase-1/ IL-1ß and eIF2α/autophagy pathway were evaluated by Western blot analysis. LC3 was assessed by immunofluorescence staining. CCH can affect cognitive function by influencing neuroinflammation, NLRP3/caspase-1/IL-1ß pathway, and eIF2α/autophagy pathway. Past exposure to cigarette smoke can also affect cognitive function by influencing neuroinflammation and NLRP3/caspase-1/IL-1ß pathway, which may be induced by smoking and may not be alleviated after smoking cessation. Past exposure to cigarette smoke does not influence autophagy, which may be increased by smoking and then decrease to normal levels after smoking cessation. Past exposure to smoking can further aggravate cognitive impairment and neuroinflammation in VaD animals: cognitive impairment induced by CCH via neuroinflammation, NLRP3/caspase-1/IL-1ß, and eIF2α/autophagy pathway and cognitive impairment induced by past exposure to cigarette smoke via neuroinflammation and NLRP3/caspase-1/IL-1ß pathway. The combined group had the worst cognitive impairment because of harmful reasons.