リンゴ斑点落葉病菌が生成するAM毒素の二つの初期作用点とその病理的意義

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  • Two Primary Action Sites for AM-toxin Produced by Alternaria alternata Apple Pathotype and Their Pathological Significance.
  • リンゴ斑点落葉病菌が生成するAM毒素の二つの初期作用点とその病理的意義〔英文〕
  • リンゴ ハンテンラクヨウビョウキン ガ セイセイスル AM ドクソ ノ フタツ

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A host-specific toxin (AM-toxin) produced by Alternaria alternata apple pathotype has two primary action sites: plasma membranes and chloroplasts where the toxin induces electrolyte loss and inhibition of photosynthetic CO2 fixation, respectively. AM-toxin I at a concentration of 10-8M caused an increase in electrolyte loss and an inhibition of CO2 fixation as well as necrosis in susceptible apple leaves. Electrolyte loss and necrosis in moderately resistant apple and Japanese pear leaves were induced at 10-5M, while CO2 fixation was significantly inhibited at 10-7-10-6M. Furthermore, CO2 fixation was affected at the concentrations of 10-6-10-5M in resistant and some non-host leaves, without causing electrolyte loss and necrosis. AM-toxin induced infection with avirulent spores in susceptible and moderately resistant leaves at 10-7 and 10-5M, respectively. However, 10-5M AM-toxin I did not show the infection-inducing activity in resistant and non-host leaves. SH-reagents such as iodoacetamide gave a remarkable protection against AM-toxin-induced electrolyte loss and necrosis formation in susceptible leaves, only when the leaves were treated before toxin exposure. On the contrary, the inhibition of photosynthetic CO2 fixation induced by the toxin was not affected by the reagent. When susceptible leaves pre-treated with the reagent were inoculated with virulent spores, the spores failed to invade the tissues. These results indicate that a role of host-specificity factor of AM-toxin I is dependent on toxin action to plasma membranes rather than chloroplasts, and hence, an accessibility of cells for invading fungi necessitates the plasma membrane dysfunction caused by the toxin.

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