저항성 유도물질(acibenzolar-S-methyl)처리에 의한 토마토 잿빛곰팡이병 발병억제

Abstract

병 저항성 유도물질인 acibenzolar-S-methyl[benzo(1,2,3) thiadiazole-7-carbothioic acid-S-methyl ester, ASM]을 토마토 유묘에 처리하여 잿빛곰팡이균(Botrytis cinerea)에 대한 유도저항성 여부를 조사하였다. 병원균 접종전 ASM 처리구에서는 병원균의 균사생장 뿐만 아니라 발병율도 현저히 감소하였다. 접종 3일전에 토마토 유묘에 처리한 ASM은 잿빛곰팡이병에 대한 균사생장억제(46.5%)와 함께 최고 55%의 발병 억제효과를 나타냈다. 한편, 토마토 유묘내 저항성 정도를 구명하기 위하여 ASM 처리에 의한 peroxidase의 활성을 측정하였다. ASM 처리된 조직 세포내에서는 현저하게 효소의 활성이 증가하였는데, 이러한 결과는 병원균을 미접종한 처리구 보다 접종 처리구에서 훨씬 크게 증가하였다. 그러나, 대조구인 물 처리구에서는 효소의 활성이 나타나지 않았다. 따라서, ASM 처리구내 병원균의 균사생장 및 발병억제는 조직세포내 산화적, 항산화적 보호시스템의 활성이 증가하였기 때문으로 판단된다. The plant defence activator, Acibenzolar-S-methyl [benzo (1,2,3) thiadiazole-7-carbothioic acid-S-methyl ester, ASM] was assayed on tomato seedlings for its ability to induce resistance against Botrytis cinerea, the causal agent of gray mold in tomato. Pre-treatment of plants with ASM reduced the severity of the disease as well as the growth of the mycelium in plants. In ASM treated plants, reduction in disease severity (up to 55%) was correlated with suppression of mycelia growth (up to 46.5%) during the time course of infection. In plants treated with ASM, activities of peroxidase were determined as markers of resistance. Applications of ASM induced Progressive and significant increase of the enzyme in locally treated tissues. Such responses were expressed earlier and with a much higher magnitude when ASM-treated seedlings were challenged with the pathogen, thus providing support to the concept that a signal produced by the pathogen is essential for triggering enhanced synthesis and accumulation of the enzymes. No such activities were observed in water-treated control plants. Therefore, the slower symptom development and reduction in mycelium growth in ASM treated plants might be due to the increase in activity of oxidative and antioxidative protection systems in plants.