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Kerry MaguirePhD student, University of Nottingham |
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The eyespot pathogens Tapesia yallundae and T. acuformis infect the stem base of wheat and other cereal crops. Disease lesions formed at these sites disrupt nutrient and water translocation and predispose the plant to lodging. Eyespot is a serious disease of cereals, especially winter wheat, in many temperate regions of the world.
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![]() | Eyespot lesion at stem base (left) and lodging caused by eyepot disease in a plot of wheat (right) |
We have been investigating the infection process of Tapesia and the factors leading to tissue and host specificity.
Spores initially germinate on and penetrate the coleoptile, and then form multicellular infection plaques on the underlying leaf sheaths. The developmental process leading to the formation of these infection structures was studied by light, confocal and electron microscopy. Induction of plaques in vitro was assessed on artificial substrata differing in hydrophobicity and topography. Plaques did not form on any surface or particular topography tested, or in response to nutrient starvation. Instead, plaques were strongly induced when the mycelium was sandwiched between two surfaces. Mechanical pressure is therefore the stimulus for plaque formation in T. yallundae.
The stretch-activated calcium channel inhibitor GdCl3 strongly reduces plaque formation under inductive conditions in a manner similar to GdCl3 inhibition of thigmotropic responses in rust fungi. This suggests that a novel mechano-stimulus is transduced in the same way as thigmotropic recognition of surface topography. Application of mechanical pressure to fungal mycelium or germinating spores on other parts of the host, e.g. leaves, or on non-host plants, induced plaque formation and penetration. Therefore the localisation of eyespot pathogenesis to the stem base may be determined by the sensory environment at the infection court as well as factors such as tissue susceptibility.
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![]() | GFP-tagged T yallundae growing in wheat leaf (left) and stem (right) visualised by confocal microscopy. Under normal conditions the eyespot fungus does not infect the leaf lamina, but in this experiment a mechanical stimulus was applied to spores on leaves, inducing infection plaques and invasion of tissues. |
Eckert, M., Maguire, K., Urban, M, Foster, S., Fitt, B., Lucas, J., Hammond-Kosack, K.E. (2005) Agrobacterium tumefaciens-mediated transformation of Leptosphaeria spp. and Oculimacula spp. with the reef coral gene DsRed and the jellyfish gene gfp. FEMS Microbiological Letters 253: 67-74.
Mueller E, Bailey A, Corran A, Michael AJ, Bowyer P. (2001) Ornithine decarboxylase knockout in Tapesia yallundae abolishes infection plaque formation in vitro but does not reduce virulence toward wheat. Molecular Plant Microbe Interactions 14: 1303-1311.
Wood, H.M., Dickinson, M.J., Lucas, J.A. and Dyer, P.S. (2001) Cloning of the CYP51 gene from the eyespot pathogen Tapesia yallundae indicates that resistance to the DMI fungicide prochloraz is not related to sequence changes in the gene encoding the target site enzyme. FEMS Microbiology Letters 196: 183-187.
Bowyer, P, Mueller,E., and Lucas J. (2000). Use of an isocitrate lyase promoter-GFP fusion to monitor carbon metabolism of the plant pathogen Tapesia yallundae during infection of wheat. Molecular Plant Pathology 1: 253-262.
Lucas,J.A., Dyer,P.S. and Murray, T. D. (2000) Pathogenicity, host-specificity, and population biology of Tapesia spp., causal agents of eyespot disease in cereals. Advances in Botanical Research 33: 226-258.
Dyer, P.S., Hansen, J., Delaney, A. and Lucas, J.A. (2000) Genetic control of resistance to the sterol 14α-demethylase inhibitor fungicide prochloraz in the cereal eyespot pathogen Tapesia yallundae. Applied and Environmental Microbiology 66: 4599-4604.