Recognition and Response in Plant/Fungus Interactions

Resistance to plant pathogens: possible roles for free polyamines and polyamine catabolism

“…Stakman (1915) originally described hypersensitivity as a rapid, localized necrosis of host cells at the infection site. This hypersensitive response (HR) can occur in response to an avirulent pathogen, in interactions involving race‐specific resistance, as well as in many examples of nonhost resistance (Heath, 1989; Mansfield, 1990; Mansfield et al ., 1997) and is characterized by the rapid death of a limited number of cells in the vicinity of the invading pathogen (Heath, 2000). Subsequent signalling events are assumed to coordinate local and/or systemic activation of an array of defence responses, which play a role in resistance (Morel & Dangl, 1997).…”

Isolation of Arabidopsis genes that differentiate between resistance responses mediated by the RPS2 and RPM1 disease resistance genes.

“…In the interaction of Arabidopsis with Peronospora parasitica, many pairs of resistance genes and fungal avr genes have been defined, and severa1 morphologically distinct phenotypes of hypersensitive lesions have been observed in different incompatible interactions (Holub et al, 1994). Microscopic studies of many plant-funga1 interactions have shown that the action of different resistance genes inhibits fungal colonization at various stages of infection (Mansfield, 1990). In the P syringae-Arabidopsis system, the timing of the HR mediated by avrRpt2 or avrRpm7 is different, and characteristic timing of the HR has also been noted in other resistance gene-avr gene interactions (Mansfield et al, 1994).…”

Hrp Mutant of Pseudomonas syringae pv phaseolicola Induces Cell Wall Alterations but Not Membrane Damage Leading to the Hypersensitive Reaction in Lettuce

“…The occurrence of membrane damage, necrosis, and collapse of challenged cells have now been established as common features of the HR, but the early stages of the response remain poorly defined. In particular, the relationship and possible coordination between the induction of membrane damage and activation of other responses such as modification of the cell wall and phytoalexin synthesis are still incompletely understood (Lamb et al, 1989;Mansfield, 1990;Marco et al, 1990;Slusarenko et al, 1991;Mansfield et al, 1994;Mehdy, 1994). The HR occurring in response to fungal infections is often highly localized; for example, the response of lettuce (Lactuca sativa) cultivars to the downy mildew fungus Bremia This work was supported by a studentship from the Agricul-lactucae is confined to individual penetrated cells (Woods et al, 1988).…”

“…The HR occurring in response to fungal infections is often highly localized; for example, the response of lettuce (Lactuca sativa) cultivars to the downy mildew fungus Bremia This work was supported by a studentship from the Agricul-lactucae is confined to individual penetrated cells (Woods et al, 1988). In consequence, biochemical analyses of early events during fungal infections are difficult to interpret because responses occurring in comparatively few cells may be masked by a background of unaffected tissue (Mansfield, 1990;Bailey, 1982;Bennett et al, 1994). Because of the spatial and temporal difficulties associated with an examination of the HR induced by fungi, the most detailed knowledge of biochemical and ultrastructural events occurring in cells undergoing the HR has come from work on plant-bacterium interactions in which comparatively large amounts of responding tissue may be obtained (Brown and Mansfield, 1988;Adám et al, 1989;Croft et al, 1990;Marco et al, 1990).…”