Abstract
Ethylene was rapidly produced in sweet potato root tissue in response to infection by black rot fungus (Ceratocystis fimbriata). We have already shown that major sources of ethylene synthesis in the infected tissue may originate from a pathway independent of methionine-ACC pathway.Inhibitors of NADPH oxidase, phospholipase, lipoxygenase, hydroxyl radical and metalions significantly suppressed ethylene synthesis in sweet potato root tissue induced by infection with the fungus. Inhibition by metal ion chelators was restored by the application of cupric ion. These results suggestthat in sweet potato root tissue in response to fungal invasion, unsaturated fatty acids released from membrane phospholipids are hydroperoxidized by lipoxygenase. The resultant hydroperoxy compounds could be degraded in the presence of reactive oxygen species and cupric ion (or copper enzyme), giving rise to ethylene. De novo protein synthesis was required for ethylene synthesis to be induced in the infected tissue.
