Abstract

Pathogenesis in diseases caused by vascular wilt fungi depends upon the entry of the organism into the xylem of the host, and its continued spread through the vascular system, although other conditions may have to be fulfilled before symptoms are expressed. Mechanisms which reduce the probability of the pathogen entering the xylem, or which limit the extent or intensity of vascular colonization, will contribute to wilt resistance. A number of such mechanisms operating in the prevascular phase (primary determinants) and in the vascular phase of pathogenesis (secondary determinants) have three features in common: they are non-specific and can be induced in many plants by many fungi; they can be induced by minor damage to cells or tissues; and their effectiveness depends upon the rate of response of a process involving synthesis of cell material or other metabolites. The formation of ethylene has been demonstrated during pathogenesis in certain vascular wilt diseases; it is suggested that ethylene at appropriate low concentrations may function as a ‘trigger’ for some of the determinant mechanisms of resistance, but that at high concentrations it contributes to pathogenesis by accelerating processes of senescence. It is suggested that wilting, as such, is an incidental feature of the vascular wilt syndrome and not of fundamental significance.

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