Plant Infectin Mechanisms of Alternaria Pathogens : Non-Host Defense Peactions and Their Regulation by Host-Specific Toxins

基本概念of The host recognition and initial colonization in host cells by Alternariapathogens that produce host-specific toxin (s) (HST) on spore germination have been established asfollows:1) Release of a signal HST from germinating spores of the pathogen，pathogen's signal by putative receptors in host cells，3) foment of accessibility to attempted fungal penetration in host cells through transduction ofthe signal. Lines of evidence for supporting this hypothesis have collected. New host-specifictoxins, ACT-toxins I and IIisolated from spore germination fluids of the tangerine pathotype of Alternaria和elucidated in structure as poly-hydroxyoctenoylvalyl esters of epoxy-decatrienoic acid. Thistrienoic acid is the common moiety of ak and af toxins. In addition，ACT-toxin II is 5" deoxy derivative of toxin I；hence,a structureactivity correlation study was possible. a candidate protein for HST receptor wasdetected. Toxin action processes comparatively analyzedcell death self not necessary for conditioning the accessible state and the results showed that cell death self not necessary for conditioning the accessible statehost cells to fungal invasion. Rather，HST suppresses general defense reactions such as production and/or accumulation ofinfection factors or lignification in infection sites that was elicited by “Inducer”40000 daltons sugars released by fungal spores. Our experiments suggest that HST-dependingAlternaria infection definitely differs from the mechanism of necrotrophic parasitism。

The basic concept of the host recognition and initial colonization in host cells by Alternaria pathogens that produce host-specific toxin (s) (HST) on spore germination have been established as follows :1) Release of a signal HST from germinating spores of the pathogen, 2) recognition of pathogen's signal by putative receptors in host cells, and 3) foment of accessibility to attempted fungal penetration in host cells through transduction of the signal. Lines of evidence for supporting this hypothesis have been collected. New host-specific toxins, ACT-toxins I and II, were isolated from spore germination fluids of the tangerine pathotype of Alternaria alternata and elucidated in structure as poly-hydroxyoctenoylvalyl esters of epoxy-decatrienoic acid. This trienoic acid is the common moiety of AK- and AF- toxins. In addition, ACT-toxin II is 5"-deoxy derivative of toxin I ; hence, a structure-activity correlation study was possible. A candidate protein for HST receptor was detected. Toxin action processes were comparatively analyzed, and the results showed that cell death itself is not necessary for conditioning the accessible state of host cells to fungal invasion. Rather, HST suppresses general defense reactions such as production and/or accumulation of infectionーinhibiting factors or lignification in infection sites that was elicited by "Inducer", 40000 daltons sugars released by fungal spores. Our experiments suggest that HST-depending Alternaria infection definitely differs from the mechanism of necrotrophic parasitism.