ABSTRACT Transmission electron microscopy was used to study the penetration and infection of pansy roots by Thielaviopsis basicola. Events observed in 7- to 10-day-old roots produced on moist filter paper differed slightly from those in roots from 4-week-old plants washed free of potting media prior to inoculation. By 3 h postinoculation (PI), epidermal cells of roots produced on filter paper exhibited aggregated cytoplasm and papilla formation in response to germ tube tips. The presence of callose in papillae was demonstrated using immunogold labeling. Papilla formation was not effective in preventing host cell penetration. A slender infection hypha emerged from a germ tube tip and grew through a papilla. Its tip then expanded to form a globose infection vesicle. By 6 h PI, infection hyphae emerged from infection vesicles, and invaded host cells showed signs of necrosis. By 8 h PI, infection hyphae had grown into cortical cells in spite of papilla formation in these cells. By 24 h PI, distinctive intracellular hyphae were present in necrotic cortical cells. In washed roots, most epidermal cells failed to respond to invasion. Hyphae simply grew through these cells and contacted cortical cells that exhibited aggregated cytoplasm and papillae formation. Infection structures similar to those produced in epidermal cells from roots grown on filter paper then formed in cortical cells of washed roots. The fact that T. basicola formed infection structures only in cells that responded to invasion suggests that T. basicola has a more complex relationship with its host than would be expected in a nectrotrophic pathogen. We believe that T. basicola is best described as a necrotrophic hemibiotroph.
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http://dx.doi.org/10.1094/PHYTO.2000.90.8.843 | DOI Listing |
FASEB J
January 2025
Department of Medicine, Hematology and Oncology, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.
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Neurodegeneration and Repair Lab, Department of Pathology, Postgraduate Program in Anatomical Pathology, Faculty of Medicine, Universitary Hospital Clementino Fraga Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
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Department of Anesthesia, Fujian Medical University Union Hospital, Fuzhou, China.
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Centre for Research in Neuroscience, Brain Repair and Integrative Neuroscience Program, Department of Neurology and Neurosurgery, The Research Institute of the McGill University Health Centre, Montreal, QC H3G 1A4, Canada.
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State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Department of Pathology, Xijing Hospital and School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
Isocitrate dehydrogenase (IDH) mutations frequently occur in lower-grade gliomas and secondary glioblastomas. Mutant IDHs exhibit a gain-of-function activity, leading to the production of D-2-hydroxyglutarate (D-2HG) by reducing α-ketoglutarate (α-KG), a central player in metabolism and epigenetic modifications. However, the role of α-KG homeostasis in IDH-mutated gliomagenesis remains elusive.
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