6 research outputs found

    Studies On The Survival Of Microsclerotia Of Verticillium Dahliae

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    The soilborne plant pathogen Verticillium dahliae Kleb. produces numerous multicellular, melanized resting structures called microsclerotia (MS) inside senescing host tissues. Melanin has been implicated in the long-term survival of fungal resting structures in soil. A method for the laboratory production, isolation, harvest and storage of stable populations of MS was developed and a procedure for plating individual MS was used to quantitatively measure both lethal and sub-lethal treatment effects. MS of 75-106 {dollar}\mu{dollar}m size exhibited faster and more synchronous germination, produced larger colonies and survived long term storage at 24 C better than MS of 53-75 {dollar}\mu{dollar}m or {dollar}{dollar}35 weeks at 24 C. UV irradiation of albino MS for 2 h severely inhibited germination (a lethal effect) and reduced colony size (a sublethal effect). Melanized MS survived better than melanin deficient MS when buried in soil. TCZ treated MS buried in various soils often gave rise to colonies which were not V. dahliae, implicating soil microorganisms in the reduction of their survival. Inoculation of soil with Talaromyces flavus or Trichoderma aureo viride reduced the survival of melanized and TCZ treated MS to 51% and {dollar}\u3c{dollar}10% or 79% and {dollar}\u3c{dollar}14% respectively after 5 weeks burial. A possible mycoparasite isolated from MS (Penicillium sp.) reduced the survival of melanized and TCZ treated MS to 73% and {dollar}\u3c{dollar}20% respectively. The addition of bloodmeal (BM) to soil at 1% w/w eradicated melanized MS and reduced the infection of eggplants with V. dahliae from 90% to 20%. Within 15 days of adding BM the soil pH rose from 5.5 to 8.2 and returned to original levels after 25 days. Since MS suspended above BM amended soil were killed within 6 days, a volatile fungitoxic factor (possibly ammonia) was implicated. Burial of MS in soil amended with 1% w/w urea or 0.5% ammonium acetate completely inhibited germination but 1% ammonium sulphate had no effect

    UNBOUND

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    Featured here, are the extraordinary works of our graduating Fashion Design class. This accomplishment is truly a celebration of the tree years of passion, hard work, and dedication of our students. It\u27s our hope that the fashion industry will partake in the creative endeavors of the emerging designers from the Fashion Design program at Fanshawe College in London, Ontario.https://first.fanshawec.ca/famd_design_fashiondesign_unbound/1002/thumbnail.jp

    Abstracts of papers presented at the Sixth InternationalVerticillium Symposium Abstracts of papers presented at the Seventh Conference of the Entomological Society of Israel

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    Genetic determinants of risk in pulmonary arterial hypertension: international genome-wide association studies and meta-analysis.

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    BACKGROUND: Rare genetic variants cause pulmonary arterial hypertension, but the contribution of common genetic variation to disease risk and natural history is poorly characterised. We tested for genome-wide association for pulmonary arterial hypertension in large international cohorts and assessed the contribution of associated regions to outcomes. METHODS: We did two separate genome-wide association studies (GWAS) and a meta-analysis of pulmonary arterial hypertension. These GWAS used data from four international case-control studies across 11 744 individuals with European ancestry (including 2085 patients). One GWAS used genotypes from 5895 whole-genome sequences and the other GWAS used genotyping array data from an additional 5849 individuals. Cross-validation of loci reaching genome-wide significance was sought by meta-analysis. Conditional analysis corrected for the most significant variants at each locus was used to resolve signals for multiple associations. We functionally annotated associated variants and tested associations with duration of survival. All-cause mortality was the primary endpoint in survival analyses. FINDINGS: A locus near SOX17 (rs10103692, odds ratio 1·80 [95% CI 1·55-2·08], p=5·13 × 10-15) and a second locus in HLA-DPA1 and HLA-DPB1 (collectively referred to as HLA-DPA1/DPB1 here; rs2856830, 1·56 [1·42-1·71], p=7·65 × 10-20) within the class II MHC region were associated with pulmonary arterial hypertension. The SOX17 locus had two independent signals associated with pulmonary arterial hypertension (rs13266183, 1·36 [1·25-1·48], p=1·69 × 10-12; and rs10103692). Functional and epigenomic data indicate that the risk variants near SOX17 alter gene regulation via an enhancer active in endothelial cells. Pulmonary arterial hypertension risk variants determined haplotype-specific enhancer activity, and CRISPR-mediated inhibition of the enhancer reduced SOX17 expression. The HLA-DPA1/DPB1 rs2856830 genotype was strongly associated with survival. Median survival from diagnosis in patients with pulmonary arterial hypertension with the C/C homozygous genotype was double (13·50 years [95% CI 12·07 to >13·50]) that of those with the T/T genotype (6·97 years [6·02-8·05]), despite similar baseline disease severity. INTERPRETATION: This is the first study to report that common genetic variation at loci in an enhancer near SOX17 and in HLA-DPA1/DPB1 is associated with pulmonary arterial hypertension. Impairment of SOX17 function might be more common in pulmonary arterial hypertension than suggested by rare mutations in SOX17. Further studies are needed to confirm the association between HLA typing or rs2856830 genotyping and survival, and to determine whether HLA typing or rs2856830 genotyping improves risk stratification in clinical practice or trials. FUNDING: UK NIHR, BHF, UK MRC, Dinosaur Trust, NIH/NHLBI, ERS, EMBO, Wellcome Trust, EU, AHA, ACClinPharm, Netherlands CVRI, Dutch Heart Foundation, Dutch Federation of UMC, Netherlands OHRD and RNAS, German DFG, German BMBF, APH Paris, INSERM, Université Paris-Sud, and French ANR

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