By R. Heitefuss (auth.), R. K. S. Wood (eds.)

A NATO complex research Institute on "Active Defence Mechanisms in vegetation" was once held at Cape Sounion, Greece, 21 April - three could 1981. It succeeded an analogous Institute held at Porte Conte, Sardinia in 1975 on "Specificity in Plant ailments. " What are lively defence mechanisms within the context of plant sickness during which a plant, the host, could be broken through a pathogen? Defence mechanisms include houses of the host that lessen this harm. The mechanisms are passive after they are self sustaining of the pathogen. they're energetic once they persist with adjustments within the host brought on by the pathogen. therefore for a fungal pathogen, mobile partitions of a better plant that are lignified earlier than an infection will be a passive defence mechanism in the event that they lowered harm by means of impeding progress of the fungus. telephone partitions identified to develop into lignified as a reaction to the pathogen will be an energetic defence mechanism if it have been verified that this reaction reduced harm. The papers and discussions at this complex examine Institute have been approximately energetic defence mechanisms in greater vegetation, regularly econo­ mically vital crop vegetation, opposed to fungi, micro organism and viruses as pathogens. Taking the microorganisms first it's a truism yet one who bears repeating that even if vegetation quite often develop in shut organization with a large choice of fungi and micro organism, usually of varieties that may be pathogens, they hardly turn into diseased, not less than no longer sufficiently on the way to allure notice.

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The initial conclusion that phytoalexins were of host origin was based on the demonstration that phytoalexins were produced in tissues after treatment with various chemicals, as well as after infection with a range of fungi and bacteria (18, 20). Since that time many more chemicals and also short-wave irradiation (59) and nematodes (40) have also been found to be effective. Other important discoveries were that fungal culture filtrates and extracts of mycelial walls could cause phytoalexins to be formed.

The many possibilities have been discussed in detail by Ingram (21). It is a sobering thought that more than sixty years after the publication of Stakman's paper in 1915 we still do not know for certain whether rapid host cell death really does have a role to play in the resistance of any host to any biotrophic fungus, let alone what that role might be (48). Real progress will only be made when : (a) many more genetically defined host-parasite combinations have been examined; (b) there has been closer integration of structural and metabolic studies; and (c) 'rapid cell death (hypersensitivity)' and 'limitation of fungal growth' have been better defined in both structural and biochemical terms.

28. J. C. (1979). Histology and physiology of compatibility and incompatibility between lettuce and the downy mildew fungus Bremia lactuaae Regel. Physiological Plant Pathology 14, 291 - 312. 29. S. (1975). Autoradiography and fine structure of host-parasite interface in temperature-sensitive combinations of wheat stem rust. Phytopathologische Zeitschrift 82, 207 - 215. 30. MARRYAT, D. (1907). Notes on the infection and histology of two wheats immune to the attacks of Puecinia glumaraum~ yellow rust.

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