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Cytological and pharmacological evidence that biotrophic fungi trigger different cell death execution processes in host and nonhost cells during the hypersensitive response
Institution:1. Keck Graduate Institute, Claremont, CA, USA;2. Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA, USA;1. Department of Biology and CESAM, University of Aveiro, 3810-193 Aveiro, Portugal;2. School of Medicine, University of St Andrews, Medical and Biological Sciences Building, North Haugh, St Andrews, United Kingdom;1. Research Center of Natural Resources of Chinese Medicinal Materials and Ethnic Medicine, Jiangxi University of Traditional Chinese Medicine, Nanchang, PR China;2. Department of Chemical and Pharmaceutical Engineering, College of Chemical Engineering, Huaqiao University, Xiamen, 361021, Fujian Province, PR China;1. Plant Molecular Biology and Biotechnology Research Center, Gyeongsang National University, Jinju, 660-701, South Korea;2. Division of Applied Life Science (BK21 Plus Program), Gyeongsang National University, Jinju, 660-701, South Korea;3. Department of Plant Bioscience, Life and Industry Convergence Research Institute Pusan National University, Miryang, 627-706, South Korea;4. Department of Plant Microbe Interaction, Max Planck Institute for Plant Breeding Research, Carl-von-Linné-Weg 10, Köln 50829, Germany;5. National Institute of Crop Science, Rural Development Administration, Suwon 441-857, South Korea;1. Department of Mycology and Plant Pathology, Institute of Agricultural Sciences, Banaras Hindu University, Varanasi, India;2. Department of Plant Science, University of Manitoba, Winnipeg, MB R3T 2N2, Canada;3. Department of Biochemistry and Immunology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil;4. Molecular Glycobiotechnology Group, Discipline of Biochemistry, School of Natural Sciences, National University of Ireland Galway, Galway, Ireland
Abstract:Living epidermal cells undergoing a hypersensitive response to penetration by a rust or a powdery mildew fungus exhibited two distinct patterns of cellular changes that occurred from the time of the cessation of cytoplasmic streaming to protoplast collapse. In nonhost cells, this death process was completed in less than 1 h, trans-vacuolar strands initially remained visible after streaming stopped, Brownian-like motion was seen in particulate cytoplasmic components, and the plant nucleus was usually associated with the intracellular fungus. In resistant host cells, trans-vacuolar strands disappeared as cytoplasmic streaming stopped, no motion was seen in the cytoplasm, there was no consistent association of the plant nucleus with the fungus, and the death process took 2 h or more. Neither type of cell death was mimicked by the application of CuCl2, salicylic acid, or KCN, nor did the individually distinctive morphological features of the cell deaths that they triggered change with chemical concentration. Pharmacological studies suggested that host and nonhost cell death required an influx of extracellular calcium, protein kinase activity and protein synthesis, but not the generation of extracellular reactive oxygen species. The application of peptides with an RGD motif delayed cell death in only one resistant host, and inhibitors of caspase activity delayed cell death only in the nonhost combinations. These and other results suggest that some rust- and powdery mildew-specific resistance genes in host cultivars may control a different cell dismantling process during the hypersensitive response than that triggered in nonhost plants.
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