Publication | Closed Access
Ecological implications of recognition events in the pre‐infection stages of root pathogens
53
Citations
60
References
1996
Year
EngineeringPlant PathologySummary Host‐specificityBacterial PathogensPlant-pathogen InteractionHost SpecificityRoot-soil InteractionRecognition EventsPathogen TransmissionRoot SystemRoot PathogensFixed PointParasitologyHost-pathogen InteractionsFungal SymbiosisRecognition SystemsFungal PathogenBiologyEcological ImplicationsMicrobiologySymbiosisHost ResistanceMedicine
Summary Host‐specificity and recognition by root‐infecting pathogens are reviewed, with emphasis on fungi but drawing parallels with other root parasites, symbionts and rhizosphere micro‐organisms. Two major levels of specificity are identified: family‐specific parasitism, exemplified by many parasites that characteristically infect Gramineae, and the possibly recent segregation of pathogen species into crop‐specific strains. In both of these cases there are examples where host‐specificity is paralleled by host‐recognition in the pre‐infection stages, including host‐specific triggering of propagule germination. The pre‐infection sequence of zoosporic pathogens (Pythium, Phytophthora, Aphanomyces spp.) is reviewed. These fungi seem to have both general (low‐affinity) and host‐specific (high‐affinity) receptor‐based recognition systems for chemotaxis to root diffusates and for induction of encystment by host surface components. Zoospores orientate (dock) during encystment, and the cysts germinate from a fixed point, whereas the non‐motile spores of at least some root parasites (e.g. Idriella bolleyi) can germinate from any point, which is influenced by the host. The possession of both general and host‐specific recognition systems by a parasite could enable it to exploit rhizosphere niches or to invade compromised plants in the absence of preferred hosts. Evidence from graminicolous (family‐specific) Pythium spp. suggests that host‐specific recognition is quantitative rather than absolute but, when compounded over successive cycles of infection, is a powerful selective mechanism.
| Year | Citations | |
|---|---|---|
Page 1
Page 1