Showing papers on "Phytoalexin published in 1969"

Role of a phytoalexin in controlling lesion development in leaves of Viciafaba after infection by Botrytis spp

Abstract: SUMMARY Phytoalexin extracted from infection droplets and diseased tissues behaved as an ether-soluble acid, and was easily separated by solvent partition from other ether-soluble substances. The phytoalexin was formed in leaves by apparently healthy cells in advance of hyphae of either Botrytis fabae or B. cinerea, and in response to physical injury. Concentrations of phytoalexin around deep lesions caused by B. fabae were completely fungistatic. B. fabae caused apparent degradation of phytoalexin in lesions, and removed phytoalexin from solutions in vitro much more readily than did B. cinerea. The lower sensitivity to the phytoalexin, and the possibly related greater ability to metabolize the phytoalexin, are major factors in the greater pathogenicity of B. fabae than of B. cinerea. The same properties largely explain the ability of B. fabae to cause the so-called ‘aggressive’ phase of the chocolate-spot disease under some conditions.

Physiology of disease resistance in sugarcane with particular reference to red rot

Abstract: Resistance to fungal and bacterial diseases of sugarcane is a hypersensitive reaction (HR). Meristematic tissues do not respond with HR; therefore, though present in differentiated cells, HR is not useful against root rot which destroys the root tips. Resistance against this disease is an exclusion phenomenon depending on the actinomycete and fungal flora of the rhizosphere. HR in red rot is related to the speed of activation of polyphenol oxidase (PPO) and this in turn is affected by temperature. On juvenile leaves, following germination of spores of an avirulent strain of the red rot pathogen, diffusates contain a factor (a phytoalexin) inhibitory to the germination of other spores. Dormant infections in bud scales and leaf-scar tissue is associated with partial resistance. Accumulation of phenolic aglycones in sublethal concentrations in host cells in response to infection induces formation of dormant structures of the pathogen. Higher temperatures (Ca 32° C.) favour development of avirulent types, whereas at lower temperatures virulent types persistin vivo. Rapid degeneration of the pathogen and greater host resistance at higher temperatures explain the infrequency of red rot in tropical areas; the reverse favours the frequent epiphytotics in sub-tropical areas.